Local Anasthesia.pdf

Local Anesthesia: Types Nerve Fibers A- Myelinated (very fast ,example: bers) - Varying diameter & function - Saltatory conduction B- Unmyelinated - Smallest diameter e.g. C bers - Sequential depolarization C...

Local Anesthesia: Types Nerve Fibers A- Myelinated (very fast ,example: bers) - Varying diameter & function - Saltatory conduction B- Unmyelinated - Smallest diameter e.g. C bers - Sequential depolarization C- Internal structure – Myelinated - Mantle bers - Core bers Propagation of Action Potential Resting cell membrane potential - -70mV - Slightly permeable to Na+ - Freely permeably to K+ & Cl- Rapid depolarization occurs - Increased permeability to Na+ - Membrane potential increases by ~15mV (-55mV) Otherwise depolarization does not occur Repolarization - Absolute refractory period – no action potential can be initiated - Sodium channels in inactivated state - Relative refractory period – can re but needs a larger stimulus - Sodium channels slowly convert back to closed state until most in this state once resting potential re-established 1 of 19 fi fi fi fi fi  Trigeminal N. - have sensory, Motor, Parasympathetic innervation, and special sensory innervation - Largest cranial nerve with three divisions A- Sensory to the dura mater & cerebral blood vessels, most of the scalp, the face, oral, nasal cavities TMJ & teeth B- Carries proprioceptive impulses from the masticatory, facial & extraocular muscles. C- Motor to the masticatory muscles, the anterior belly of digastric, mylohyoid, tensor veli palatini & tensor tympani. *Deliver P. sympath. & special taste from other nerves to the end organ *The only branch that is motor : Mandibular branch Maxillary N (V2) (good for botox) - Leaves the cranial cavity through the Foramen Rotundum - Passes across the Pterygopalatine Fossa - Enters the orbit through the Inferior Orbital Fissure - Passes through the Infraorbital Groove & Canal emerging into the face Principal branches of the maxillary division v2 In the cranial cavity (cranial): Meningeal nerve (supplies the middle cranial fossa) In the pterygopalatine fossa (Maxillary N.): Ganglionic branches which pass through the pterygopalatine ganglion (without synapsing!), which include: - Greater palatine nerve, Innervates palatal tissue from premolars to soft palate. Lies 1cm medial to 2nd molar region - Lesser palatine nerve, mucous membranes of the soft palate & parts of the tonsillar region - Nasopalatine nerve - Pharyngeal branch-exits the pterygopalatine ganglion & travels through the pharyngeal canal, innervates mucosa of the portions of the nasopharynx - PSA, prior to entrance in to infraorbital groove innervates posterior maxillary alveolus, periodontal ligament, buccal gingiva & pulpal tissue molars ?MB 1ST. molar) - Orbital branch supplies periosteum of the orbits - Nasal branches- supplies mucous membranes of sup & middle conchae, lining of post ethmoid sinuses, & post nasal septum. - Nasopalatine nerve- travels across the roof of nasal cavity giving branches o to the ant. nasal septum & oor of nose. Enters incisive foramen & provides palatal gingival innervation to the premaxilla - Zygomatic nerve: - ZF,skin to cheek prominence - ZT, skin to lateral forehead - pre ganglionic : by V1 (opthalmic N.) - Post ganglionic: by V2 (Maxillary N.) —>gives the secretomotor innervation of lacrimal gland - Communicating branch to Lacrimal N. to provide postganglionic P.Sym. Secretomotor innervation to the lacrimal gland. In the infraorbital canal (Infraorbital N.): Middle & anterior superior alveolar nerves Facial branches: Inferior palpebral- lower eyelid External nasal- lateral skin of nose Superior labial branch- upper lip skin and mucosa (CHECK THE FIGURES IN PAGE 4) 2 of 19 fl ff Mandibular N. (V3) - Largest branch of the trigeminal nerve - Leaves the cranial cavity through the Foramen Ovale as separate motor and sensory roots - The roots joint to form the Mandibular Nerve - Divides into a small Anterior Trunk and a larger Posterior Trunk - The Posterior Trunk ends by entering the Mandibular Foramen, emerging into the face through the Mental Foramen - Sensory root: Originates at inferior border of trigeminal ganglion - Motor root: - Arises in motor cells located in pons & medulla oblongata - Lies medial to the sensory root - Carries P. symp. & special taste via lingual (submandibular & Otic ganglia & chorda tympani Facial n. CN7) * we usually anesthetize IAN, if u want to extract L6 ( IANB , Lingual N, buccal N) anterior belly is supplied by Mandibular N, Post belly is supplied by facial. * Do u know how botox work? It blocks acetylcholine ( a neuroreceptor) cholinergic , acts on nicotinic and muscarinic receptors — which acts on muscle, sympathatic ,parasympathetic so. if u inject botox upper close to upper eyelid, what u will have ? ptosis (upper eyelid drop) a ecting a very important muscle that is called Pretarsal muscle in. orbicularis oculi muscle ( ssure ,diamond shape), supratarsal muscle innervated only by sympathetic N. if people have upper eye drop and u inject sympathetic memic drug, they will gain some of that muscle function *submandibular gland receives and get secretomotor innervation parasympathetic by chorda tympani via lingual N by a pathway ( Pre-ganglionic chorda tympani of facial N enter infra- temporal fossa and then joins Lingual branch bers of mandibular N—>pot ganglion —> innervate sublingual and subandibular gland). * The parotid gland gets it from Otic ganglion via auriculotemporal on pathway of (glossopharyngeal N —> Lesser petrosal N —> Otic ganglion —> auriculotemporal branch of CN V3 Mandibular N. Principal branches of the mandibular division V3: Cranial: - Meningeal nerve (Nervus Spinosus), re-enters cranial cavity through foramen Spinosum along with the middle meningeal artery, supplies ant., middle cranial fossae & the mucous lining of the Mastoids cells through its post. branch - Nerve to medial pterygoid (supplies medial pterygoid, tensor tympani & tensor Veli palatini) ANTERIOR TRUNK Buccal nerve Masseteric nerve (supplies masseter) Deep temporal nerves (two nerves, supply temporalis) Nerve to lateral pterygoid (supplies lateral pterygoid) POSTERIOR TRUNK: Auriculotemporal n., sensory to TMJ & Otic ganglion for sensory, secretory, & vasomotor to Parotids Lingual n. Inferior alveolar n.àN. to mylohyoid (supplies mylohyoid & ant. belly of digastric) Mental n. Incisive n. 3 of 19 fi ff fi 4 of 19 Local Anesthesia: - The pH has to be acidic between 3.5-5.5 pH for the following reasons: - maximize stability in solution and shelf-life - Solubility: LA solutions are aqueous solutions, its pH is close to 7.4 the lipid soluble uncharged form could precipitate out due to its lower water solubility - Stability: the uncharged base form is more unstable at physiological pH, therefore degradation is minimized at low pH where the drug is predominantly in the charged form - Stability of Adrenaline: it’s unstable at physiological pH and more stable in acidic pH - Shelf-life is 3-4 years. - Hydrochloride acid is what added to achieve acidic drug. Content of LA: LA agent: Conduction blockade Vasoconstrictor: Dec. abs of LA into blood, thus inc. duration of ansthsia + dec. systmc toxicity Increase potency & decrease bleeding Sodium metabisul te: Antioxidant for vasoconstrictor, most likely it is the cause of allergy in LA. Methylparaben: Preservative to inc. shelf life; bacteriostatic, also can cause allergic reaction Sodium chloride: Isotonicity of solution Sterile H2O: Diluent Needle: - Gauges: 25g, 27g, 30g. (The higher the number the lesser the diameter) - Length: Short (26mm), Long (36mm) - Prefer to use longer and smaller diameter (high gauge, less painful) Local Anesthetic classi cation: - Esters: A:Benzoic acid B: Para-aminobenzoid acid (PABA) hypersens. - Amides - Quinoline: Centbucridine LA Chemical Con gurations: - An Aromatic lipophilic ring - Ester or amide linkage - A hydrophilic 2nd or tertiary amino group, which forms water soluble salts when combined with acids (HCl) 5 of 19 fi fi fi  Amides Mepivicaine (Carbocaine): conc. 3%. used in very acidic , infected tissue bcz it has High pKa Lidocaine (xylocaine): 2%, 1%, 1.8 is the volume of lidocaine carpule Articaine (Septanest), (amide+easter)! Bupivacaine (Marcaine): the longest acting in comp. to all LA , due to high protein binding (95) and pKa. More potent long duration. Used for spinal anesthesia. Very toxic to the HEART Prilocaine (Citanest) risk of Methemoglobinemia Esters: - mainly for kids, eyedrops - Cocaine, Tetracaine, Procaine (injectable), Benzocaine (topical) - Hydrolyzed in plasma by Plasma Pseudocholinesterase - if patient have low plasma pseudocholinesterase —> it lingers the time of this LA in blood - Metabolized into PABA & excreted in urine - 1/3000 have atypical Pseudocholinesterase: - Prolonged neuromuscular blockade - Can be low levels or atypical enzyme (genetic) - Atypical forms identi ed by LA-dibucaine-inhibits normal plasma cholinesterase to a greater extent (20%) than a typical enzyme Mechanism of Action of LA Class C (most of LA used in the clinic) Displacement of calcium ions from nerve receptor site Binding of local anesthetic molecule to this receptor site. Blockade of the sodium channel —> prevents Action potential Decrease in sodium conductance May a ect impulse of nerve in one of the following ways: Alter resting potential Alter threshold potential Decrease rate of depolarization Increase duration of repolarization Mechanism of Action - Speci c receptor theory: LA binds to speci c receptor on the Na+ channel 1. Displacement of calcium ions from the sodium channel receptor site 2. Binding of the local anesthetic molecule to this receptor site 3. Blockade of the sodium channel 4. Decrease in sodium conductance 5. Causing: - Depression of depolarization - Failure to achieve threshold potential - prevention of propagated action potentials - Conduction Blockade Causing = Conduction blockade LA can alter nerve conduction at 4 sites with Na+ channel Outer surface of Na+ Channel – Biotoxins (tetrodotoxin, saxitoxin) Within Na+ Channel – Amide LAs At the activation or inactivation gate on internal surface of nerve membrane - scorpion venom, quaternary analogs of lidocaine Receptor-independent physio-chemical mechanism - Benzocaine All local anesthetics have three main components: 1. Lipophilic aromatic ring 2. Ester or amide linkage 6 of 19 fi ff fi fi  3. Tertiary amine Anesthetic potency —> Determined by the aromatic ring group and the tertiary amine. Greater lipid solubility leads to greater di usion through nerve sheaths and neural membranes More Facts: - Concentration/volume injected # of molecules can a ect the duration and onset - Most of the LA cause vasodilation Concaine: - The most potent vasoconstrictor - Cocaine cause initial vasodilation then vasoconstriction - people who take cocaine through there mouth and nose , su er from something related to vasoconstriction (perforated palate and more commonly perforated nasal septum, due do vasoconstriction and ischemia) Dissociation of Local Anesthetics - Local anesthetics are weak basic compounds – Pka – 7.5-10. Therefore Combined with hydrogen in acidic solution (HCl giving a LA salt leading to a Cation soluble in water + stable (stored with hydrochloride in suspension) - Physiologic pH- 7.4, areas of in amm. or infection pH – 5-6 - Action of LA based on: - Di usion through nerve sheath – basic form (Non-ionic & lipophilic) - Binding to receptor side in Na+ channel – Cationic form - Dissociation calculated using Henderson-Hasselbalch equation [ pH=pKa +Log base/acid ] - E ectively – the lower the tissue pH, the less dissociation into basic form = less LA available to di use across nerve membrane * To make the tissue more acidic we can inject it with BICARBONATE, increasing the basic a ect and decrease the acidity in the infected area * PKa is inversely proportional to the onset of action, The fastst is the one with pH close to body * Tetracaine and bupivacaine have higher pKa 7 of 19 ff ff ff ff fl ff ff ff  Potency & Duration * Sequence of blocking nerve bers is as follow: - External bers get numbm then small bers get numb (ex: C bers), so pain and temperature get numb rst then motor and proprioception Potency Determined by lipid solubility pKa partition coe cient Increased lipid solubility = greater potency The more potent the local, the lower the concentration (%) of local required e.g. Bupivacaine.25,.5 &.75% Duration: Determined by protein binding - ↑ protein binding = ↑ duration of action - Vasoconstrictors - Renal clearance / renal function - Hepatic breakdown / hepatic function Onset: Determined by pKa (primarily) - ↓ pKa (higher pH) = ↑ onset time (faster) because more “Non ionized form” available - Onset a ected by tissue pH (acidic environments such as abscesses have less “Non ionized form” available) will take longer and more time to work - The closer the local is to the nerve, the faster it will work as well - Non-nervous tissue permeability - {} of LA # of molecules *Lidocain with epi dose is 7 mg/kg 8 of 19 fi ff fi ffi fi fi fi Metabolism of LA Distribution - Absorbed in to blood – carried to highly perfused organs - Blood [ ] related to: Rate of absorption in to CVS Rate of distribution from vascular compartment to tissues Elimination of drug – metabolism and excretion Metabolism - Esters – hydrolyzed by pseudocholinesterase in plasma - Byproduct - PABA (source of allergic reactions) - Excreted in kidneys - Amides: P450 is very famous enzyme metabolize most of drugs - Bio transformed in the liver - Excreted in kidneys * Note: Articaine has ester linkage —> metabolized in blood & liver * Prilocaine – metabolized in liver & some in Lung Consider Medical status of pt. * Liver/kidney dysfunction – reduced metabolism/excretion à toxicity Systemic E ects of LAs Cardiovascular - CVS more resistant than CNS to local anesthetics - ropivacaine,bupivacaine are cardiotoxic - Reduced myocardial depolarization - Myocardial depression - Decrease excitability of myocardium —> decrease conduction rate and force of contraction - Lidocaine is used for patients with tachycardia - LAs may be used to treat dysrhythmias (lidocaine and procainamide) - Lido: Premature Ventricular Contractions & V. Tach - Procainamide —>SVT - Overdose —> Cardiovascular collapse - Hypotension - Vasodilation of peripheral vasculature - Percent of pts with hypotension - procaine50% vs lidocaine 6% 9 of 19 ff CNS: - Most CNS toxic = Lidocaine - Inhibit the inhabitory causes excitation —> Seizure - LAs cross blood brain barrier: No CNS e ects at concentration at risk of injecting pterygoid venous plexus. - So injection to PSA —>ptegoidvenus plexus —> high chance of sezuir after LA Systemic E ects Pre-convulsive Convulsive Respiratory depression Initial 3 signs & symptoms Peri-oral & tongue numbness (circumoral) Tinnitus Metallic taste 10 of 19 ff ff Systemic E ects of LAs Respiratory: Bronchial smooth muscle relaxation Neuromuscular blockade: May prolong e ects of Succinylcholine or Rocuronium Malignant hyperthermia: No documented cases related to amide LAs Tachycardia, tachypnea, acidosis, pyrexia/fever (up to 42 degrees C), muscle rigidity Mortality 63-73% Epinephrine: Catecholamine (Hormone)produced by the adrenal medulla Sympathomimetic ( ght-or- ight) Nonselective adrenergic α + β agonist Vasoconstrictor & bronchodilator 0.003mg/kg up to 0.2mg (in healthy patient). 0.04mg (cardiac patient) Fast onset, short duration, t1/2 about 2-3 min Metabolism: Reuptake by adrenergic nerves Mono amine oxidase (MAO) + catecholamine-o-methyl transferase (COMT) Both are hepatic forms of clearance Used in many emergencies Comes with a preservative Act indirectly by provoking the release of endogenous catecholamine from the intraneural storage sites Side notes: Used in anaphylaxis shock bcz it causes vasoconstriction and bronchodilator , status asthmatics and with cardiac arrest when someone is in stressful situation in long time and they are using ght or ight for long time, they get tachyphylaxis which means they deplete their reservoir of catecholamine , they need to be given exogenous catecholamine to stabilize. Recommended dose Healthy ASAI and II– 200ug Cardiac comorbidity ASA III and IV – 40 ug Pediatric consider 3 ug/kg Pregnancy - 100 ug Epinephrine ⍺ & β – get rebound vasodilation Phenylephrine – ⍺ only no rebound β e ects Side note: - when someone is healthy and u gave him 200 ug how soon u can give him another 200 ug ? after 1hr bcz in half an hour the rst 200ug are gone Vasoconstrictors decrease the rate of absorption by: 1. Concentrate the tissue drug level 2. Inc. duration 3. Dec. site vascularity 4. Dec. anesthetic blood level 5. Dec. systemic toxicity & potential overdose of LA 11 of 19 ff fi fl fi ff ff fi fl  LA Duration Max recommended Lidocaine (Xylocaine) 1% & 2% Medium (30-60 min) Without epinephrine: 4.5 mg/kg; not to exceed 300mg Lidocaine with epi. 1:100,00 & Long (120-360 min) With epi.: 7mg/kg 1:200,000 Mepivicaine 2% - 3% Medium (45-90 min) With epi.: 7mg/kg dose 400mg Bupivacaine 0.5 % Long (120-360 min) 2.5mg/kg; max dose 175mg (Marcaine, Sensorcaine) Bupivacaine w epi. 1:200,000 Long (180-420 min) Max dose 225mg/kg Articaine HCl 4% (Septanest, - Max dose 7mg/kg Ultracaine) 1:100,000/200,000 Prilocaine (citanest) Medium (30-90 min) 8 mg/kg 70 kg pt. max dose 600mg In ltration: – su cient in the maxilla due to the thin cortical nature of the bone – Involves injecting to tissue immediately around surgical site Supraperiosteal injections ntraseptal injections Periodontal ligament injections Intrapulpal Side notes: in the palate don’t inject too much , we don’t want necrosis due to the constrictors A field block is a method of providing anesthesia to a relatively small area by injecting a “wall” of anesthetic solution across the path of the nerves supplying the operative eld. Instead of the injection being made directly into the area of the procedure, it is made into the soft tissue some distance away, where the nerves are situated. Advantages include longer duration of anesthesia and no distortion of the operative eld Nerve Block: - Local anesthetic deposited near main nerve trunk and is usually distant from operative site Posterior superior alveolar Greater palatine Nasopalatine nferior alveolar nerve Lingual nerve Long buccal nerve Mental nerve Mandibular nerve Infraorbital Method of injection: - Squeeze the tissues as a distraction - Insert the needle through stretched mucosa - Aspirate - Inject SLOWLY Side notes: why do we try to cause dome vibration before we inject? * to make the propioception over come sensation (bigger and faster bers) * THE BEVEL SHOULD FACE THE BONE 12 of 19 fi ffi fi fi fi  Inferior Alveolar Nerve block - Muscles that are penetrated during IANB are: - buccinator - superior constrictor - palatoglossus - palatopharyngeus - you use these muscle to direct your self - Di cult with people with macroglossia , cant open their mouth, what to do? change technique to akinosi IAN Technique: * Pterygomandibular space lies between the ramus of the mandible and the medial pterygoid muscle, and below the lateral pterygoid muscle Gow-Gates Technique: * The GOW GATES technique blocks most of the mandibular division of the trigeminal nerve. The object is to place the tip of the needle by the lateral side of the condylar neck * The needle is inserted at the level of the occlusal plane, just distal to the third molar tooth, with the barrel of the syringe lying over the opposite premolars. * The needle should be advanced along a line parallel to a line connecting the corner of the mouth with the intertragic notch (incisure) of the ear, until it contacts the neck of the condyle. The AKINOSI Closed mouth mandibular block Technique: * The needle is advanced posteriorly and slightly laterally, at the level of the molar mucogingival junction about 25 mm into the tissues. The bevel should face medially, to de ect the needle more laterally. Side Notes: how to inject? let the patient close mouth completely , then go parallel to marginal gingiva , go straight and aim to hit the anterior border of the ramus , once u hit, go back a little pit go medial and inject with the whole length of the LONG needle , aspiration is essential. Also u can bend , go from same side. When patient comes with trismus —> v good technique to use it with ACCESSORY INNERVATION - This typically manifests as persistent sensitivity in a lower tooth despite having given an apparently successful inferior alveolar block. - It is due to an additional nerve supply to the tooth. The following nerves have been implicated: BUCCAL LINGUAL MYLOHYOID CERVICAL PLEXUS INFERIOR ALVEOLAR N. OF OPPOSITE SIDE Dosing considerations: - Patient with cardiac history: - Should limit dose of epinephrine to 0.04mg - Most local anesthesia uses 1:100,000 epinephrine concentration (0.01mg/ml) - Pediatric dosing: - Clark’s rule: Maximum dose = (weight child in lbs/150) X max adult dose (mg) Use in Pregnancy: - Local anesthetics – Category B or C b/c all LAs & vasoconstrictor cross placenta - Attempt to limit Epi to 0.1mg - Lidocaine Safe for preg / Etidocaine SAFe and used as aspinal anesthesia during delivery - Risk of Fetal bradycardia – Bupivacaine & Mepivacaine - Topical Benzocaine & Tetracaine + injectable Prilocaine may have risk of Methemoglobinemia 13 of 19 ffi fl  Cocaine & Amphetamines - Cocaine peak blood levels 30 min after use and last for 4-6 hrs - Methamphetamine - peak 3-5 min, duration is 8-12 rs - Plasma t1/2 is 12-34 hrs (if use 12 hrs then ~75% eliminated after 24 hrs) - Urine detection up to 72 hrs - Sympathomimetic drug – cause NorEpi release in adrenergic nerve terminals may exert action on ⍺ & β - Vasoconstrictor use may cause tachycardia & hypertension leading to: - Cardiac dysrhythmias - Myocardial ischemia & infarction - Cardiac arrest - Avoid within 24 hrs of Cocaine or Methamphetamine use (some may consider avoiding for 72 hrs after use Side Notes: cocaine went through long term vasoconstriction causing chronic High blood pressure they need to be treated with a speci c type of Hight blood pressure medication and that has an e ect on us. ENT drs use Cocaine alot to numb the nose , Stop bleeding. 14 of 19 ff fi Idiosyncrasy: Abnormal reaction to normal does. A patient developing CNS reaction after 1 carp. Complication: Persistent/prolonged anesthesia / parathesia IAN/Lingual N. inj. Trismus Hematoma Bleeding Infection Faint Seizure Tissue sloughing Post-anesthetic intraoral lesion/ulcer/necrosis/NSM Facial nerve Paresis/paralysis (temp.) Needle breakage Intravascular injection Needle stick inj. Also can: Provoke Herpes simplex Recurrent aphthous stomatitis Side notes: - what to do if needle breakage? Take OPG , tell not close mouth ( if u can retrieve it with an artery forceps try but make sure not to displace it further, if u cant refer - if the paralysis for 40 mins don’t do anything but if it is more we need to do something Toxicity: A phase of followed by excitation depression Clinical manifestations Fear/anxiety Restlessness Throbbing headaches Tremors Weakness Dizziness Pallor Respiratory di culty/palpitations Tachycardia ( PVCs, V-tach, V- b) Systemic Complications - Most common are Psychogenic - vasodepressor syncope - Pallor, sweating, nausea, anxiety, reduced LOC (level of consciousness), tremors - Reduced O2 perfusion - Supine/elevate legs - O2 at 10 ml/min - hyperventilation (acute hyperventilation syndrome) - Excess loss of CO2 and respiratory alkalosis - Confusion, dizziness, paresthesia of extremities, tachycardia, carpopedal spasm, N/V, - Calm breathing/breathing exercises - Breath slowly in paper bag or rebreathe mask —> Rebreathe CO2 15 of 19 ffi fi Methemoglobinemia: - Prilocaine injection or topical Benzocaine in high doses - Pts with congenital Methemoglobinemia are predisposed - Prilocaine broken down to Ortho-Toluene - Causes reduction of Fe2+ (ferrous state) to Fe3+ (ferric state) & inhibits Methemoglobin reductase (so the ferric can not donate Oxygen) - Fe3+ (ferric state) has increased a nity for oxygen = less dissociation into tissues Side notes: - the iron is changed from a status that take and donate to a status that take and hold oxygen this can happen when we use prilocaine , and even with other type of LA - Hemoglobin ise the molecule that present in the red blood cells and helps in distributing the oxygen all over the body, whereas, methemoglobin does not have the ability to release oxygen, When a patient su er from Methemoglobinemia, the hemoglobin in the body is not able to release oxygen in an e ective manner to the body tissue Signs and Symptoms , 3-4 hrs after LA use: - Cyanosis – when Methemoglobin reaches 15% (or when 5 mg per ml is methemoglobinized) - Lethargy - Respiratory distress - Syncope - Ashen skin - Death is rare – risk when concentration reaches 50-60% Most susceptible patients - Children less than 4 months as their fetal hemoglobin has not yet fully disappeared - Congenital Methemoglobin reductase (diaphorase I) de ciency - G6PD def. (X-lined trait that results in hemolytic anemia because RBCs cannot function properly) Pathophysiology Hemoglobin is oxidized to Methemoglobin Normal HEME has Ferrous ion Fe+2 which binds 4 molecules of Hb In Methemoglobinemia ferrous Fe+2 gets converted to ferric Fe+3 from oxidation Fe+3 binds O2 & does not readily give it up like Fe+2 (hence SaO2 levels stay relatively high but patients are experiencing hypoxic state) Normally Fe+3 is quickly converted back to Fe+2 to prevent hypoxia via methemoglobin reductase (cytochrome-b5 reductase) Oxygen hemoglobin curve shifts to the left Signs and symptoms: The blood is chocolate color Cyanotic pateint but saturation is often only slightly reduced (85%) Giving oxygen alone does not help Acute Management Methylene blue (1- 2mg/kg IV over 5 min) ( it is dark blue) An electron acceptor & converts Fe+3 back to Fe+2 oxygen 16 of 19 ff ff ffi fi Systemic complications - Management Preconvulsive state Monitor and reassure pt May start IV Benzo as preventative measure Tonic-Clonic Protect pt Self limiting usually 1-3 minutes as LA concentration declines Seizure > 5mins IV Midaz – titrated 1mg/min IM midaz – 0.2mg/kg of 5mg/ml concentration Intranasal – 0.2mg/kg up to 10 mg (use if less than 50 kg) Side notes: - we give IM injection of the drug of choice adavan (lorazepam) or midazolam which also works well both are from (benzodiazepine) family Cardiovascular Evidence of Severe Cardiovascular depression Severe Hypotension Reduced MAP Reduced HR Cardiac Arrest Administer Intralipid–lipid emulsion 20% solution Bolus 1.5ml/kg over 1 minute Infuse at rate of 15ml/kg/hr After5mins Give max of 2 repeat doses ( 5 mins between each) Double infusion rate Max dose of 12ml/kg Intralipid binds to lipid soluble LAs and reduces plasma concentration results in release from cardiac muscle LA Reversal Agent Intralipid cont. Contraindications Hypersensitivity to fat emulsion or components of the formulation ( severe egg or legume (soybean) allergies) Pathologic hyperlipidemia Acute Pancreatitis associated with hyperlipidemia 17 of 19  Allergic reaction: More common with ester based local anesthetics Most allergies are reactions to the preservatives in the pre-made local anesthetic carpules Methylparaben Sodium bisul te Metabisul te Side notes: The plunger can also causes allergy cause it has latex Treatment: Most over dose rxns are self limiting because blood levels in brain & heart continue to dec. as the rxn continues. Redistribution & biotransformation takes place: Stop everything ABC’s (assessed&maintained) 00% Oxygen IV & monitors Call EMS Supportive care ( uids, anticonvulsants (Benzo), BLS/ACLS Local Site Reversal: OraVerse (Phentolamine): is the best and the of choice drug to treat cocaine hypertention Non-selective ⍺ adrenergic antagonist Vasodilator Dec. BP (esp. in Cocaine HTN emerg) Useful in peds Most common adverse e ects are tachycardia, bradycardia & headache. 18 of 19 fi fi fl ff 19 of 19