Flashcards in Anaesthesia and Analgesia Deck (183):
Local anaesthetics reversibly interrupt propagation of nerve impulses by interfering with sodium ion influx into peripheral nerve cells.
Topical anaesthesia is generally less effective for mucosal surfaces.
Very effective dt enhanced absorption.
Intradermal infiltration of anaesthesia causes less pain thn subcutaneous infiltration
Other way around
Intradermal infiltration of anaesthesia is more immediate in onset and more prolonged than subcutaneous infiltration
The chemical structure of most local anaesthetic agents consists of an aromatic portion, an intermediate chain, and an amine portion.
The amine portion of the local anaesthetic compound provides most of its lipophilic properties.
The aromatic end of the local anaesthetic compound facilitates the diffusion of the anaesthetic through membranes, which correlates to the potency of the anaesthetic.
The hydrophilic end of the local anaesthetic compound is involved in binding within the sodium channel.
This is usually a tertiary amine.
The intermediate chain of the local anaesthetic compound consists of either an ester or an amide.
Amide-type compounds tend to have a shorter duration of action because they are rapidly hydrolyzed by plasma pseudocholinesterases to form metabolites excreted by the kidneys. .
This is true for esters. Pts with decreased levels of pseudocholinesterase may be prone to their toxic effects
PABA is the major metabolite product of the ester-type anaesthetics and is responsible for their higher incidence of allergies.
related to PPD - cross reacts with ester anaesthetics
suphonylureas and thiazides alos cross react with this group
Ester derivatives are metabolised by microsomal enzymes in the liver and excreted by the kidneys.
This is true for amides.
Individuals with compromised liver function are more susceptible to the toxic effects of ester anaesthetics.
This is true for amides.
Highly protein-bound anaesthetics, such as bupivacaine, are tightly associated with the neural membrane, leading to a longer duration of action.
Shorter-acting anaesthetics tend to have a longer action of onset and more toxicity.
Shorter onset of action, less toxicity.
Local anaesthetics are weak bases, with a pKa between 7.7 and 9.1.
Prepared with hydrochloride salts though so become acidic.
A lower pKa correlates to a higher concentration of base and a faster onset of action.
Tissue pH does not affect the action of local anaesthetics.
Eg. infected tissue more acidic
Local anaesthetics can cross the placenta.
Local anaesthetics can be excreted in breast milk.
Procaine, tetracaine, benzocaine, chloroprocaine, and cocaine are types of amide anaesthetics.
Lignocaine, bupivacaine, mupivacaine and prilocaine are types of ester anaesthetics.
Procaine has a faster onset of action than lignocaine.
Procaine 5 mins, lignocaine
Procaine lasts longer than lignocaine.
Procaine 15-30mins, ligno 30-120 mins.
Bupivacaine and mepivacaine last longer than lignocaine.
There is significant benefit of adding vasoconstrictors to lipid-soluble anaesthetics (bupivicaine/ropivicaine) to prolong their effect
They are already highly tissue bound
The maximum dose of adrenaline for LA should not exceed 1mg over approximately 8-10hours
The recommended maximum dose for procaine is 10mg/kg for adults, without adrenaline.
14mg/kg with adrenaline.
The recommended maximum dose for lignocaine is 7mg/kg for adults, without adrenaline.
7mg/kg with adrenaline.
The recommended maximum dose for bupivacaine is 2.5mg/kg for adults, without adrenaline.
3mg/kg with adrenaline.
The recommended maximum dose for mepivacaine is 10mg/kg for adults, without adrenaline.
8mg/kg with adrenaline.
A and B nerve fibres are myelinated and C fibres are unmyelinated.
Smaller myelinated fibres are easier to block than larger myelinated fibres, therefore pain and temperature sensation may be eliminated before the loss of vibration and pressure.
The A-alpha fibres primarily conduct light touch and pressure.
The A-beta fibres conduct motor impulses.
Light touch and pressure.
The A-gamma fibres are responsible for joint proprioception.
The A-delta fibres conduct pain and temperature. They are the smallest of the A fibres.
A fibres are the largest of the nerve fibres.
B-fibres are preganglionic sympathetic fibres.
C-fibres are the smallest and conduct pain and temperature.
All local anaesthetic promote vasodilation by relaxation of vascular smooth muscle.
Vasoconstrictors added to local anaesthetic impair the absorption of the anaesthetic and prolong its duration.
Sodium bicarbonate 10.5% is used in a dosage of 1mL for every 10mL of 1% lignocaine with adrenaline.
8.4%, to decrease pain with infiltration of acidic solution.
Full vasoconstriction with adrenaline typically requires only 30-60 seconds.
Adrenaline can reduce uterine blood flow and induce premature labour, therefore non-urgent procedures requiring the use of adrenaline should be postponed until after pregnancy.
Hyaluronidase facilitates local diffusion of anaesthetics.
Adding sodium bicarbonate to local anaesthetics allows for increased amounts of uncharged, lipid-soluble base, which more readily crosses the nerve membrane, leading to faster onset of action.
There is no need to patch test hyaluronidase prior to use.
Contains allergen thimerosal.
Hyaluronidase decreases the duration of anaesthesia and potentially increases the risk of anaesthetic toxicity as a result of increased absorption
Uniform dose of hyaluronidase is 10u/ml
There is no uniform dosage, but 150units in 20-30mls of anaesthetic has been used
Hyalmuronidase contains the preservative thimerosal which is a contact allergen
Because rare allergic reaction have been reported, preoperative skin testing has been recommended
Hyaluronidase is recommended for tumescent liposuction.
See above for why it isn’t.
Cocaine is primarily used as a topical anaesthesia in nasal surgery as a 4% and 10% solution.
Anaesthesia within 5 mins of application, lasts up to 30mins.
The recommended maximum dose of cocaine is 200mg/kg.
Use of topical benzocaine can cause contact sensitisation.
Benzocaine-containing preparations can be safely used in infants.
Risk of methaemoglobinaemia.
Lignocaine is available in a 2% and 5% gel, ointment or viscous solution.
Onset of action is 1-2 mins, duration 15-20 mins.
EMLA is a eutectic mixture of 2.5% lignocaine and 2.5% prilocaine.
Oil-in-water emulsion cream.
A eutectic mixture is a formulation that melts at a lower temperature than any of its individual components.
The depth of analgesia after 60mins of EMLA application is 5.0mm. .
3mm. 120 mins gives 5mm
EMLA should be used with caution in infants due to the risk of methaemoglobinaemia.
EMLA can be applied to eyes.
Risk alkaline injury.
LMX 5% is a topical anaesthetic containing lignocaine encapsulated in a liposomal delivery system.
LMX has a slower onset of action than EMLA.
Faster – 30min application time.
LMX has a shorter duration of action than EMLA.
LMX can be applied without the need for occlusion.
LMX use in a child weighing less than 20kg should be limited to an area less than 100cm2 for a single application.
Tetracaine, a long-acting ester anaesthetic, is available in a 0.5% solution and is used most commonly for ophthalmic procedures.
Common topical eye preparations include lignocaine
Proparacaine 0.5%, tetracaine 0.5%, benoxinate 0.25%
Topical eye preparations have an onset time of 30seconds
Field or ring block involves placement of anaesthesia circumferentially around the operative site.
Tetracaine can provide anaesthesia to mucous membranes for up to 45 mins.
An eye patch must be worn following anaesthesia to the eye to protect the cornea
Topical eye preparations usually last 15mins or longer
Local infiltration is suitable for infected or inflamed tissue
Field blocks are appropriate
Tumescent anaesthesia involves the delivery of large volumes of dilute anaesthesia (usually 0.05%-0.1% lignocaine with 1:1 000 000 adrenaline) into subcutaneous fat until it distends.
Safe upper limit of lignocaine with tumescent anaesthesia is estimated to be 35mg/kg
Warming of the tumescent solution to 104F before infiltration will reduce pain
Slower the rate of tumescent solution does not reduce the pain of infiltration
Yes, it does
Tumescent anaesthesia allows procedures to be done with minimal blood loss and avoiding the risks of GA
Postoperative analgesia is always required in patients who have been given tumescent analgesia
It provides post-op analgesia itself
Vasoconstrictors such as adrenaline should not be added to the anaesthetic agent when performing a nerve block due to the risk of vessel trauma.
It will improve haemostasis, slow absorption of anaesthetic, prolong its duration and decrease amount needed
But avoid in digits
Ester anaesthetics are most commonly used for nerve blocks
Small volumes of LA used for nerve blocks and so higher concentrations can be used
e.g. 2% lignocaine
Nerve blocks involve injecting anaesthesia adjacent to a nerve or within the same fascial compartment as the nerve to be anaesthetized.
Injection of anaesthetic into the nerve itself can cause a neuropraxia resulting in paraesthesia in the distribution of the nerve itself.
This can rarely be permanent
Peripheral nerve blocks generally have a rapid onset of action.
Takes 5-10 mins to become effective.
Peripheral nerve blocks have faster onset of action than local infiltrative anaesthesia
The supraorbital nerve provides sensory innervation to the mid-forehead, and frontal scalp to vertex.
This is true for the supratrochlear nerve.
The supraorbital nerve emerges from the supraorbital notch – at the superior orbital rim at the mid-pupillary line.
The supratrochlear nerve supplies sensation to the forehead, and frontal scalp to vertex.
This is true for the supraorbital nerve.
The supratrochlear nerve emerges above the eyebrow, approximately 1cm lateral to the facial midline and 1.5cm medial to the supraorbital nerve.
The supraorbital and sipratrochlear nerves can both be blocked by entering just lateral to the supraorbital notch in the mid-pupillary lines and injecting 1-mls toward the midline
The external nasal nerve supplies sensation to the dorsum, tip and alar of the nose.
Dorsum, tip and columella.
The external nasal nerve emerges at the junction of the upper lateral cartilage and nasal bones.
The infraorbital nerve supplies sensation to the contralateral lower eyelid, nasal sidewall, upper lip, medial cheek, upper teeth and maxillary gingiva.
The infraorbital nerve emerges at the infraoribtal notch in the mid pupillary line, approximately 1cm inferior to the lower orbital rim and superolateral to the nasal ala.
The infraorbital nerve can be blocked using the intraoral approach – the needle is advanced through the gingival buccal sulcas at the apex of the canine fossa
The mental nerve supplies the lower lip and cheeks.
Lower lip and chin.
The mental nerve emerges mid-height of the mandible, in the midpupillary line, approximately 1cm inferior to the second premolar.
Blocking the mental nerve provides anaesthesia to the ipsilateral chin and lower lip, but does not include its adjacent mucosa and gingival
It does include adjacent mucosa and gingival
The auriculotemporal nerve supplies sensation the the posterior auricle, angle of mandible and submandibular areas.
This is true for the greater auricular and transverse cervical nerve.
The auriculotemporal nerve emerges just superior to the temporomandibular joint at the zygomatic arch.
The greater auricular and transverse cervical nerves supply sensation to the temporal scalp, anterior auricle and lateral temple.
This is true for the auriculotemporal nerve.
The greater auricular and transverse cervical nerves emerge at Erb’s point.
The greater auricular nreve innervates the ipsilateral angle of the jaw to the submandibular area and posterior auricle
The external nasal nerve is a branch of the anterior ethmoidal nerve.
The infraorbital nerve is the smallest branch of the maxillary nerve (V2).
Using an intraoral approach for the infraorbital nerve block, the needle is advanced through the gingival buccal sulcus at the apex of the canine fossa for approx. 1cm, at which point 1-2mL of anaesthetic is injected just over periosteum.
The intraoral approach for the infraorbital nerve block is more painful
The mental nerve is a terminal branch of the mandibular nerve (V3)
The position of the foramen of the mental nerve does not vary with age.
The foramen lies closer to the upper margin of the mandible in older patients.
With the intraoral route for the mental nerve block, the anaesthetic is injected into the inferior labial sulcus between the lower first and second premolars, injecting 1-2mL just over periosteum.
The auriculotemporal nerve is a branch of the maxillary nerve (V2).
Mandibular nerve (V3).
The auriculotemporal nerve runs deep and posterior to the temporomandibular joint before it emerges superficially to travel with the superficial temporal artery.
The auriculotemporal nerve block is performed by palpating for the TMJ with the jaw open and injecting 2-3mL superior to the joint over periosteum at the zygomatic arch.
The transverse cervical nerve arises approximately 1cm superior to the greater auricular nerve.
Two dorsal and two ventral nerves lie along the lateral aspects of the digits and innervate each digit.
Addition of adrenaline to digital nerve blocks is generally not recommended because of the risk of vascular compromise.
The dorsal approach for digital nerve blocks is more painful than entering from the palmar or plantar surface.
A total volume of 3-5mL of lignocaine typically provides adequate anaesthesia for a digital block.
With digital nerve blocks pressure from the injection of excessive volumes (>8mls) can compromise the vascular circulation
Complications from nerve blocks are rare, but care must be taken to avoid digital ischaemia
Factors that contribute to the development of digital gangrene following a nerve block include: adrenaline, ring block technique (circumferential anaesthesia), excessive tourniquet pressure and postoperative burns.
Adrenaline use in digital blocks should be avoided in patients with severe hypertension, peripheral vascular and vasospastic disease, and connective tissue disease.
The median and ulnar nerves, and superficial branch of the radial nerve, provide sensation to the palm.
The median nerve is located in the midline of the volar side of the wrist between the palmaris longus tendon and the flexor carpi radialis.
Having the patient place the thumb and last two digits together accentuates the palmaris longus tendon.
Injecting 1-2mL of anaesthetic just to the radial side of the palmaris longus tendon and under the flexor retinaculum at the proximal crease of the wrist will block the median nerve.
Use 3-5ml anaesthetic. Everything else is true. This will anaesthetise most of the radial side of the palm.
The ulnar nerve runs beneath the flexor carpi ulnaris tendon and inserts into the pisiform bone.
Flexing the wrist in a slightly ulnar direction helps identify the flexor carpi ulnaris tendon.
For an ulnar nerve block, anaesthetic is injected just radial to the flexor carpi ulnaris tendon at the proximal crease of the wrist at the ulnar styloid process.
The radial nerve lies on the medial border of the radius just dorsal to the radial styloid.
Blocking the superficial branch of the radial nerve provides anaesthesia to the palmar surface of the thumb.
A radial nerve block is performed by infiltrating anaesthetic in the area lateral to the radial artery, extending toward the dorsum of the wrist.
Four nerves provide sensory innervation to the foot. They are all derived from the sciatic nerve (the tibial, the superficial and deep peroneal nerves, and the sural nerve).
Five nerves – 4 from sciatic nerve, 1 from femoral nerve (saphenous nerve).
The posterior tibial nerve innervates the plantar surface of the foot.
Except for small areas on the lateral (sural nerve) and medial (saphenous nerve) aspects.
The superficial peroneal, sural, saphenous and deep peroneal nerves innervate the dorsal aspect of the foot.
To block the posterior tibial nerve, anaesthetic is injected at the level of the upper half of the medial malleolus, posterior to the posterior tibial artery pulse and anterior to the calcaneal tendon.
The sural nerve is blocked by injecting anaesthetic 1-1.5cm distal to the tip of the lateral malleolus.
The saphenous nerve is blocked by injecting anaesthetic lateral to the saphenous vein and anterior to the medial malleolus.
Medial to the saphenous vein.
Injecting anaesthetic midway between the anterior tibial surface and the lateral malleolus provides anaesthesia to a large proportion of the dorsal foot.
The deep peroneal nerve supplies a large portion of the foot.
Only the first web space.
You should not use a digital nerve block if there is infection or trauma of the proximal phalanx (distal to the infection site)
To prevent methemoglobinaemia you should avoid using prilocaine and benzocaine in patients with risk factors
Risk factors for methemoglobinaemia include concomitant oxidant drugs such as dapsone, nitroglucerin, nitrates, nitrites, phenacetin, sulphonamides, primaquine
Prilocaine and benzocaine should be avoided in patients with risk factors for methaemoglobinaemia.
Systemic toxicity to local anaesthetics primarily affects the CNS and CVS.
Local injections of phentolamine 0.5mg/mL and topical application of nitroglycerin can reverse adrenaline-induced digital vasospasm.
Adrenaline reactions from local anaesthetic are associated with decreased blood pressure, whereas anaphylactic reactions are associated with increased blood pressure.
Other way around.
Psychogenic attacks in response to LA can manifest as vasovagal episodes and lead to lightheadedness, diaphoresis, nausea, syncope, bradycardia and hypotension
The interaction of TCAs and adrenaline may lead to hypertension, tachycardia and arrhythmias.
The interaction of beta-blockers and adrenaline may lead to hypertension followed by bradycardia.
Adrenaline should be avoided in patients with hyperthyroidism, severe hypertension, and phaeochromocytoma.
Allergic reactions to LA occur more commonly with amides than esters.
Esters more commonly. They are metabolised to the potential allergen PABA.
Management of anaphylactic reaction include administration of 03-0.5mg adrenaline subcut, BLS and transport to an acute care facility
Cross-reactions may occur among ester-type LA and PPD hair dyes, sulfonylureas and thiazides.
There is potential cross-reaction between ester and amide LA.
The use of preservative-free lignocaine is recommended if there is a clear history of procaine or PABA sensitivity.
Since lignocaine contains preservative methylparaben (related to PABA).
Concurrent use of medications that inhibit cytochrome p450-3A4 enzyme can potentially result in systemic toxicity when used in conjunction with amide-type LA.
Early symptoms of lignocaine toxicity include drowsiness and circumoral paraesthesia.
Progresses to lightheadedness, restlessness, irritability.
Higher concentrations of lignocaine can cause muscle twitching, nystagmus, blurred vision and confusion.
Seizures and cardiac toxicity generally do not occur until plasma concentrations of lignocaine approach 5mg/mL.
10mg/mL. increasing blood levels cause coma and respiratory arrest.
In healthy patients, increased blood pressure and arrhythmias generally don’t occur if the dose of adrenaline is limited to 1mg.
0.5mg (50mL of 1:100 000 dilution).
Patients with underlying systemic diseases (eg hyperthyroidism, cardiac disease, PVD and phaeochromocytoma) may be more sensitive to adrenaline.
Maximum recommended dose for these patients is 0.2mg (20mL of 1:100 000 dilution)
Higher toxic blood levels of lignocaine lead to vasodilatation, hypotension and bradycardia.
Progress to CVS collapse and cardiac arrest.
With lignocaine, signs of CNS toxicity usually do not manifest until after signs of CVS toxicity.
Other way around.
More potent LAs, eg bupivacaine and etidocaine, appear to be more cardiotoxic than other LAs.
Lignocaine and etidocaine are the LAs most commonly associated with clinically significant methaemoglobinaemia.
Benzocaine and prilocaine.
Infants and children are at greater risk of metHb than adults because haemoglobin F is more susceptible to oxidation, newborns have lower levels of reductive enzymes, and the dose tends to be greater per kilogram body weight.
Methaemoglobinaemia presents with cyanotic appearance of the skin, lips and nail beds at metHb levels of 40-50%.
Concomitant administration of other methemoglobin-forming drugs such as sulphonamides and antimalarials can increase the risk of methaeoglobinaemia
Symptoms of methaemoglobinaemia will occur at the time of LA administration.
Occur 1-3hrs following Rx, because its caused by metabolites of the LA.
Conventional pulse oximeters are reliable in detecting metHb.
Use blood gases and blood metHb levels.
High levels of metHb >30% may need iv methylene blue 1-2mg/kg as a 1% solution.
Methylene blue is contraindicated in patients with G6PD deficiency.
Give ascorbic acid 300-1000mg/day iv in 3-4 doses.
The recommended maximum dosages of lignocaine for children over 3yo are 1.5-2mg/kg for lignocaine without adrenaline and 3.0-4.5mg/kg for lignocaine with adrenaline.
For infants 0-3mo or or less than 5kg, the maximum total dose of EMLA is 1g to an area 10cm2 maximum, with an maximum application time of 1hour.
For adults, the maximum total dose of EMLA is 10g, to a maximum application area of 100cm2, for 4 hours.
20g, 200cm2, 4 hours.
Field or ring blocks may be used for areas such as the scalp, nose and pinna of the ear.
A scalp block can be performed by injecting LA approximately 4-5cm apart starting at the mid-forehead extending circumferentially toward the occiput and back around to the mid-forehead.
An ear ring block provides anaesthesia to the entire ear.
Not concha or external auditory canal.