4 main causes of pulpal inflammation

PULPITIS. DIFFERENTIAL nDIAGNOSTICS

 

Is inflammation of dental npulp tissue.

The pulp contains the nblood vessels the nerves and connective tissue inside a tooth and provides the ntooth’s blood and nutrients.

Pulpitis is mainly ncaused by bacteria infection which itself is a secondary development of caries.

 

4 main causes of pulpal ninflammation

1.      mechanical damage

2.      thermal injury

3.      chemical irritation

4.      bacterial effects (via toxins or carious lesions)

Classification of pulpitis:

 

 

Also, pulpitis can be reversible and irreversible.

Reversible pulpitis – the tooth reacts to sweetness, ncold and heat. The pain lasts for a short while only. The sensitivity test is npositive. If caries can be removed without opening the pulp, the tooth loses nits symptoms. The pulp can be kept vital. This acute form of pulpitis is ntherefore reversible.

Irreversible pulpitis – which may be acute or chronic, nthe tooth is permanently painful. The dentin is frequently destroyed up to the npulpal cavity and cariously altered. Pain continues even after caries removal nand medicamentous filling. The tooth’s sensitivity to touch and biting is njoined by decreasing or lacking reaction to a sensitivity test. The damaged npulpa cannot be reversed to its original healthy state, it is irreversible.

Classification of pulpitis:

.I. Acute pulpitis:

a.       Pulp hyperemia

b.      Traumatic pulpitis

c.       Partial (local, focal) pulpitis

d.      Diffuse pulpitis

e.       Purulent pulpitis

II. Chronic pulpitis

a.       Fibrous pulpitis

b.      Gangrenous (pulp gangrene) pulpitis

c.       Hyperplastic pulpitis (Pulp polyp, hypertrophic npulpitis) )

d.      Pulp stones (calcification, concrementous pulpitis)

III. Pulpitis, complicated with apical periodontitis

IV. Exacerbation of chronic pulpitis

 

Acute npulpitis.

In the early nstages the tooth is hypersensitive. Very cold or hot food causes a stab of paiwhich stops as soon as the irritant is removed. As inflammation progresses, npain becomes more persistent and there may be prolonged attacks of toothache. nThe pain starts spontaneously, often when the patient is trying to get to nsleep.

The pain is npartly due to the pressure on the irritated nerve endings by inflammatory ninfiltrate within the rigid pulp chamber and partly due to release of npain-producing substances from the damaged tissue. The pain at its worst is nexcruciatingly severe, sharp and stabbing in character. It is little affected nby simple analgesics.

Chronic pulpitis

The pulps of nindividual teeth are not precisely represented on the sensory cortex. The pulp npain is therefore poorly localized and may be felt in any of the teeth of the nupper or lower jaw of the affected side. Rarely, pain may be referred to a more ndistant site such as the ear. Pulp pain is not provoked by pressure on the ntooth. The patient can chew in comfort unless there is a large open cavity nallowing fragments of food to press on the pulp through the softened dentine. nMany pulps under large carious cavities die painlessly. The first indication is nthen development of periapical periodontitis, either with pain or seen by nchance in a radiograph. In other cases there are bouts of dull pain, brought oby hot or cold stimuli or coming on spontaneously. There are often prolonged nremissions.

Key features of npulpitis •

 Pulpitis is caused by infection or irritatioof the pulp, usually by caries

• Severe nstabbing pain in a tooth, triggered by hot or cold food or starting nspontaneously, indicates acute irreversible pulpitis

• Pulp pain is npoorly localised

• Chronic npulpitis is often symptomless

• Untreated npulpitis usually leads to death of the pulp and spread of infection to the nperiapical tissues Pulpal pain

The pulp may be nsubject to a wide variety of insults, e.g. bacterial, thermal, chemical, ntraumatic, the effects of which are cumulative and can ultimately lead to ninflammation in the pulp (pulpitis) and pain. The dental pulp does not contaiany proprioceptive nerve endings, therefore a ncharacteristic of pulpal pain is that the patient is unable to localize the naffected tooth. The ability of the pulp to recover from injury depends upon its nblood supply, not the nerve supply, which must be borne in mind when vitality n(sensibility) testing is carried out (p. 18).1 It is impossible to reliably nachieve an accurate diagnosis of the state of the pulp on clinical grounds nalone; the only 100% accurate method is histological section.

Although nnumerous classifications of pulpal disease exist, only a limited number of nclinical diagnostic situations require identification before effective ntreatment can be given.

Reversible pulpitis

Symptoms. Fleeting sensitivity/pain to hot, ncold or sweet with immediate onset. Pain is usually sharp and may be ndifficult to locate. Quickly subsides after removal of the stimulus.

Signs. Exaggerated response to pulp testing. Carious cavity/leaking restoration.

Rx Remove any caries present and place a sedative ndressing (e.g. ZOE) or permanent restoration with suitable pulp protection.

Irreversible pulpitis

Symptoms .Spontaneous pain which may last several nhours, be worse at night, and is often pulsatile iature. Pain is elicited by hot and cold at first, but ilater stages heat is more significant and cold may actually ease symptoms. A ncharacteristic feature is that the pain remains after the removal of the nstimulus. Localization of pain may be difficult initially, but as the ninflammation spreads to the periapical tissues the tooth will become more nsensitive to pressure.

Signs. Application of heat (e.g. warm GP) elicits pain. nAffected tooth may give no or a reduced response to electric pulp tester. Ilater stages may become TTP. 

Rx Extirpatioof the pulp and RCT is the treatment of choice (assuming the tooth is to be nsaved). If time is short or if anaesthesia proves elusive then removal of the ncoronal pulp and a Ledermix dressing can often control the symptoms until the nremaining pulp can be extirpated under LA at the next appointment.

The histopathology of pulpitis

Acute pulpitis

Early changes within the pulp from the advancing ncarious lesion involve the production of tertiary dentine by the odontoblasts. nTertiary dentine, formerly known as irregular secondary dentine, contains fewer ntubules than primary or secondary dentine. Tertiary dentine may be reactionary, nlaid down by primary odontoblasts in response to a mild stimulus, or reparative ndentine, laid down by secondary odontoblasts derived from other pulp cells. nThis attempt at a barrier to the advancing lesion can be effective if the nlesion progresses slowly and particularly so if it arrests. However, with the advancing nlesion, bacteria invade the odontoblasts and destroy the surrounding tissues. nClinically it is characterised by the patient feeling pain in response to ntemperature change which lasts for the duration of the stimulus. There is nnormally no pain on biting or when the tooth is percussed. The ninflammation of the pulp is reversible if the cause is successfully ntreated, e.g. by the removal of the caries. As the pulpal inflammatiobecomes more extensive, the pain experienced as a result of temperature change becomes nmore severe and persists after the removal of the stimulus usually for several nminutes or even longer. As the lesion approaches the pulp, inflammatory nresponses are detected in front of the advancing lesion.

Once penetration of the pulp by bacteria has takeplace, the inflammatory process becomes more profound.  The response of the tissues to this invasiois seen clinically as acute pulpitis. The inflammation produces aincrease in pressure on the walls surrounding the pulp because of the presence nof additional inflammatory cells, increased vascularity (hyperaemia) and nthe inability of the pulp chamber to expand to relieve the pressure causing the ntypical symptoms of acute pulpitis. These are:

■ A constant, throbbing pain in the affected ntooth that is

often made worse by reclining or lying down.

■ A lack of pain on biting unless the ninflammation has

spread beyond the confines of the pulp.

■ The inability to obtain relief from the npain.

Other processes which can lead to bacteria npenetrating the pulp are trauma, e.g. a fractured tooth or traumatic exposure nduring cavity preparation (iatrogenic), tooth wear, via the periodontal nmembrane or, rarely, via a bacteraemia, e.g. induced by a tooth extraction from nanother site (anachoresis).

Differential and diagnostic criteria of acute nforms of pulpitis

n

Diagnostic criteria		Diagnosis
		Pulp hyperemia	Acute localised pulpitis	Acute diffuse pulpitis	Acute purulent pulpitis	Traumatic pulpitis
Anamnesis; complaints	1	Acute spontaneous pain in affected tooth that lasts 1 – 2 min; “light periods” – 6 – 24 hrs. Pain attacks are increased at night. Pain arises from all kinds of stimuli, lasts for 1 – 2 min. after their removal. There is no irradiation of pain.	Acute spontaneous attack-like pain, lasts 5 – 10 min.; “light-periods” from 2 hrs. and more. Pain attacks are increased at night. Pain arises from all kinds of stimuli, slowly disappears after their removal. Sometimes could irradiate in adjacent teeth.	Acute spontaneous attack-like pain, from 2 hrs. and more; “light-periods” 10 – 30 min. Pain attacks are increased at night; arises from all types of stimuli in laying position. Irradiation of pain.	Spontaneous, pulsate (throbbing), continuous pain, could be weaken for a few minutes. There is a irradiation of pain. Pain is exacerbating at night and from hot stimulus; relieving factor is cold water. Any of the irritants lead to sharp attack of pain.	Accidental pulp exposure –short-termed acute pain. During crow fracture – acute pain that irradiates following branches of n. trigeminal. Pain due to all irritants even when breathing air though mouth.
Deepness of carious cavity	2	Carious cavity is medium or deep. Amount of decayed dentine is in correspondence to the course of caries.	Deep carious cavity with great amount of decayed dentine.	Deep carious cavity with great amount of decayed dentine.	Deep carious cavity with great amount of decayed dentine.	In the case of accidental pulp exposure – pink pulp is visible in one point and drop of blood comes out. In the case of traumatic fracture of tooth crown – red pulp is clearly visible.
Probing of carious cavity bottom	3	Painful in a limited part of carious cavity bottom. Pain in a few minutes disappears.	Sharply painful i one point. Pain is preserved for some time after probing is stopped.	All bottom of carious cavity is painful; pain is preserved after stopping of probing.	Sharply painful probing of all carious cavity bottom; roof of the pulp chamber could be easily perforated and drop of pus could come out.	Extremely painful
Vertical percussion	4	Painless		Painless		Painful when there is pulp exposure
Temperature test	5	Pain from cold water that lasts for 1 – 2 min.	Pain from cold or hot water that lasts for some time after irritant removal.	Pain due to cold or hot water; pai irradiates following branches of V cranial nerve.	Cold water relieve pain for few min.	Extremely painful reaction from cold or hot water.
EPT	6	8-12 mcA	15-25 mcA	20-35 mcА	35 — 45 mcА	–

 

DIFFERENTIAL DIAGNOSIS nOF PULP HYPEREMIA, ACUTE LIMITED PULPITIS

AND ACUTE DEEP DENTAL nCARIES

 

 

 

DIFFERENTIAL DIAGNOSIS nOF ACUTE SEROUS PULPITIS WITH OTHER DISEASES

 

n

Clinical signs	Diagnosis
	Acute pulpitis	Acute or exacerbation of chronic apical periodontitis	Acute maxillary sinusitis	Neuralgia of trigeminal nerve (V)
Character of pain	Sharp spontaneous, throbbing pain, increases at night and from all kinds of irritants, has irradiation of pain following branches of nerve trigeminal	Constant dull pain, increases during biting	Constant dull and throbbing pain in the maxilla, increases when head is bowed down	Throbbing, exhausting pain that appears and disappears spontaneously.
Provoking factors of pain	Temperature stimuli provoke pain, after eliminatio of irritant pain is gradually decreased.	Mastication and biting on the tooth	Any irritants don’t initiate or relieve pain. Pain could start when biting on teeth that are localized close to inflamed part of maxillary sinus.	Mechanical and temperature stimuli that do its action in triggering zones.
Additional clinical signs	Probing of carious cavity bottom is sharply painful. There is no disclosure of tooth cavity. Percussion is painful in the course of purulent pulpitis.	Probing of carious cavity bottom is painless; tooth cavity is disclosed; percussion cause sharp pain; muco-buccal fold is swallowed and hyperemic near causative tooth	Feeling of nasal congestion; difficulty of nasal breathing through appropriate half of nose; mucous or pus discharge from nose.	Hyperemia of face, tearing, increase of salivation. Reflector contraction of chewing muscle.
General state of patient’s health	Headache and weakness is possible.	Headache, weakness, loss of appetite, raise of temperature is possible.	Increase body of temperature total weakness, headache that increases during cough sneezing, tilting of the head. Quick fatigue (tiredness).	General state of organism is not changed. But during attack of pain patient freezes in troubled pose, and afraid to move.

 

 

DIFFERENTIAL DIAGNOSIS OF CHRONIC FIBROUS nPULPITIS WITHOUT TOOTH CAVITY DISCLOSURE

n

Clinical signs	Diagnosis
	Chronic fibrous pulpitis	Acute deep caries	Acute limited serous pulpitis
Character of pain	Dull pain, arises only from stimuli; absent at night	Acute, short-termed pain, arises from all kinds of stimuli	Sharp, spontaneous, throbbing pain, increases from stimuli and at night.
Duration of pai attack	Lasts for 30 – 40  min. after removal of irritant	Short-termed pain, stops immediately after removal of irritant	During a day could be a few  short attacks of pain with long “light-periods”
Anamnesis of disease	Previously there was acute or dull long-lasting pain	There was no sharp pain in past	Acute pain that arose for the first time during present day.
EPT	30-40 mcA	10-15 mcA	15-20 mcA
X-ray data	Enlargement of periodontal crevice	There is no changes in periodontium

 

 

 

DIFFERENTIAL AND nDIAGNOSTIC CRITERIA OF CHRONIC GANGRENOUS PULPITIS AND CHRONIC APICAL PERIODONTITIS

n

 

DIFFERENTIAL AND nDIAGNOSTIC CRITERIA OF CHRONIC FORMS OF PULPITIS

 

 

 

Pulp gangrene

 

–         nthe pulp ntissue due to infection and death or pulp necrosis secondary to infection of nthe pulp tissue called the pulp gangrene corruption decomposition

 

Complaints:

–         nPain from all nirritants, esp. from hot (water, hot air)

–         nPatient feel nbetter with cold

–         nUnpleasant nsmell from a tooth

–         nPain ianamnesis

–         nGrey or browcolor

–         nElectric pulp ntest – 60-100 mcA

–         nTooth can be npainless, just changed in color

 

 

Pulp gangrene

 

Chronic hyperplastic pulpitis (pulp polyp)

The pulp polyp is typically found nin the primary second molar or permanent first molar, because these teeth are nmore likely than others to be  ngreatly destroyed by caries at an age when the apical blood flow ninto the tooth is still very good.

This means that it is largely a ndisease of the first decade of life, although later lesions do occur.

It is rarely seen after 20 years nof age.

 

–         nAs a usual nasymptomatic

–         nBleeding from ndamaged area during chewing

–         nTaste of iroin the mouth

–         nMasticatory nstress can lead to some tenderness

–         nThe polyps ncover the entire cavity by enlarging itself

 

 

Chronic nconcrementous pulpitis (pulp stones)

Pulp stones are tough, nbone similar structure that develop in the pulp of a ntooth, possibly within the tooth crown or perhaps within the tooth root canal.

Pulp stones are very nfrequent, manifesting in up to ninety percent of individuals between the fifty and nseventy years.

Their occurrence nappears to raise with age.

The elements nassociated with the progression of the pulp stones are mostly unidentified.

Biological method of ntreatment is aimed at reducing the inflammation and renewing of pulp function. nSurgical method of treatment envisage total or partly removal of pulp from npreviously anaesthetized tooth or extraction of pulp after using devitalized nsubstances.

 

n

CONSERVATIVE (BIOLOGICAL) METHOD     A — indirect pulp capping; B — direct pulp capping; 1— calcium hydroxide lining; 2 — temporary dressing. Indication. Initial stages of acute pulpitis: pulp hyperemia, acute limited pulpitis, traumatic pulpitisт (accidently pulp exposure) and chronic fibrous pulpitis without clinical and Rtg signs of apical periodontitis. This method is preferable to use when: patient is younger than 30 years old; carious cavity has central location, patient don’t suffer any general diseases and there is no pathological changes i periodontium, short period of inflammation (not longer than 3 days).
SURGICAL METHOD
VITAL AMPUTATION Indication: pulp hyperemia, acute limited pulpitis, chronic fibrous and hypertrophic pulpitis, acute and chronic forms of pulpitis of temporary teeth in the period of roots resorption and i permanent teeth in the stage of root formation. Pulp amputation is indicated to old-aged patients with sclerosed and obliterated root canals and whe roots are severely curved. Anaesthetised tooth cariously exposed     Roof of pulp chamber is removed Coronal pulp is removed using slowly rotating large rose-head bur A pledget of cotton wool moistened with hydrogen peroxide is applied to the radicular pulp for 4 minutes.   The cotton with hemostatic liquid is removed and the cavity is dried and lined with zinc oxide eugenol (calcium hydroxide) and the tooth is subsequently restored with temporary dressing.	VITAL EXTIRPATION Indication: traumatic pulpitis (acute trauma with fracture of tooth crown), acute diffuse pulpitis, acute purulent pulpitis, chronic hypertrophic pulpitis (pulp polyp), chronic gangrenous pulpitis, chronic calcified pulpitis (pulp stone). Schematic diagram representing stages of vital extirpation: 1 — before treatment (carious lesion on the proximal surface, tooth previously anaesthetized); 2 — carious cavity preparation; 3 — tooth cavity disclosure; 4 — pulp amputation; 5 — enlargement of root canal orifice; 6 —pulp extirpation; 7 — determination of canal length; 8 — instrumental treatment of root canal; 9 — medicament treatment of root canal; 10 — root canal sealing using canal filler and paste; 11 — final crown restoration.

 

n

Devitalized methods of treatment
Devitalized amputation	Devitalized extirpation
This method of treatment is of rare use today in modern dentistry. Indication: 1. Treatment of pulpitis in molars with severely curved roots, thus endodontic treatment of root canals is hard. 2. Treatment of pulpitis in old-aged patients (with somatic disorders) when root canals are sclerosed and obliterated. 3. Treatment of pulpitis in patients with allergy to anesthesia.	Devitalized extirpation is indicated to patients with allergy to anesthetic solutions.   Devitalized extirpation is held in 2 appointments: 1-st appointment – pulp is devitalized using devitalizing agents (arsenic paste, paraformaldehyde paste); 2-d appointment – pulp extirpation is done with a following appropriate instrumentation and medicament treatment of root canal.

 

Main symptoms of npulpitis

The characteristic nfeature of pulpitis it is sharp, spontaneous pain with irradiation that usually nincreases at night. There are usually attacks of pain, arising spontaneously; nsometimes pain is provoked by temperature, chemical or mechanical stimuli, with na duration of pain for a few minutes after stimuli stops its action (for nopposite to caries – pain stops immediately after elimination of irritant).

Duration of paidepends on the intensity of irritant, level of pulp tissue inflammation and ncapacity of organism to manage diseases.

One of the maicharacteristic feature of pain due to pulpitis it is npresence of short periods without pain, so called “light periods”. Attacks of npain could be short with long “light periods” or long periods of pain attack nwith short “light periods” depending from level of pulp inflammation.

Purulent inflammatioof pulp is accompanied by long lasting sharp attack of pain without “light nperiods”. Pain could be weaken by rinsing oral cavity nwith cold water.

Pain could be nlocalized or irradiate following V cranial nerve (nerve trigeminal) branches.

From affected nmaxillary tooth pain could irradiate to adjacent teeth, temporal part of head nand forehead (following II division of nerve trigeminal).

From affected mandible ntooth pain irradiate into occipital part of head and ear.

It is characteristic nthat spontaneous, stabbing pain is increased at night, during dreaming, wheall outer irritants are excluded.

 

 

 

 

Anesthesia

 

General anesthesia (GA) A controlled state of nunconsciousness, accompanied by a partial or complete loss of protective nreflexes, which may include inability to maintain an airway independently and nto respond purposefully to physical stimulation or verbal command.

Deep sedation A controlled state of depressed nconsciousness, from which the patient is not easily aroused. It may be naccompanied by a partial loss of protective reflexes, including the inability nto continually maintain a patent airway independently and respond appropriately nto physical stimulation or verbal command.

Conscious sedation Sedation in which nprotective reflexes are normal or minimally altered. The patient remains nconscious and maintains the ability to independently maintain an airway and nrespond appropriately to verbal command. Conscious sedation also includes the nuse of other sedative agents and/or premedication in combination with nitrous noxide-oxygen.

Nitrous oxide-oxygen sedation Conscious nsedation accomplished solely by the use of nitrous oxide-oxygen.

 

Analgesia The loss of the sense of pain, nwithout the loss of consciousness.

Anesthesia The loss of feeling or sensation, nespecially the loss of the sensation of pain.

 

Indications, contraindications, and commosense

When dealing with LA, GA, and sedatives, ntechniques, indications, and contraindications are often relative, and the nfollowing should be thought of as guidelines rather than immutable laws.

LA The technique of choice for simple nprocedures or when a GA is C/I. LA is C/I in

•          uncooperative npatients (of any description);

•          infectioaround the injection site;

•          patients nwith a major bleeding diathesis; and

•          most nmajor surgery.

Adverse reaction to LA is a C/I, but ireality once allergy to preservatives in the solution is excluded, LA allergy nprobably does not exist.

Conscious sedation

This is an extension of LA technique using ndrugs and patient-management techniques. It is of benefit to anxious or mildly nuncooperative patients and is a kind supplement to apicoectomy or third-molar nremoval. C/I include the following:

•          Cardiorespiratory, nrenal, liver, or psychiatric pathology

•          Aunescorted patient or one unable or unwilling to conform to the requirements of nconscious sedation (p. 582)

•          A ndemonstrated adverse reaction to sedative agents

•          Pregnancy, nduring which benzodiazepines should be avoided

GA Indicated when LA or LA and sedation is nineffective or inappropriate (as above). C/I include the following:

•          All nthose for conscious sedation

•          Presence nof food or fluid in the stomach (most anesthesiologists require at least 4 h nbetween last feed and GA)

The anesthesiologist usually prefers hospital nadmission for patients with the following:

•          Cardiovascular nor respiratory disease (especially MI <6 months ago)

•          Uncorrected nanemia, sickle cell trait or disease

•          Severe nliver or renal impairment

•          Uncontrolled nthyrotoxicosis or hypothyroidism

•          Poorly ncontrolled diabetes, adrenocortical suppression

•          Malignant nhyperthermia

•          Pregnancy

•          Neurological ndisorders, e.g., myopathy or multiple sclerosis

•          Cervical nspine pathology such as rheumatoid arthritis or cervical spondylosis

•          Certaidrugs, e.g., steroids, antihypertensives, MAOIs, anticoagulants, narcotic nanalgesics, antiepileptics (need to avoid using methohexitone), lithium, and nalcohol. Malignant hyperthermia, succinylcholine apnea, and other unwanted nreactions to anesthetic agents

•          Causes nof upper airway obstruction such as angioedema, submandibular cellulitis, nLudwig’s angina, and bleeding diathesis affecting the neck (In fact, these are nindications to secure the upper airway.)

•          Previous nproblems with anesthesia

Ask about previous GA and any problems. Note drugs nused, as repeated administration of halothane may induce hepatitis and should nbe avoided within a 3-month period. While all these conditions create problems nwith anesthesia, they may not preclude it absolutely within the hospital nsetting. They do, however, indicate the need for careful assessment and early nprior consultation with the anesthesiologist.

 

Local anesthesia—tools of the trade

While any disposable-needle and syringe system ncan be used to give LA, the vast number of LAs given in dental practice n(>50,000/dentist/lifetime) has led to some very useful modifications.

LA cartridges Supplied in 1.8 ml carpules, nthey are presterilized. The most common solution used is lidocaine 2% with nepinephrine 1:100,000. A latex-free version is available for patients with nlatex allergy.1

Cartridge syringes Use with above, they are nsterilizable and used with disposable needles. Needles are available i25ga-long, 25ga-short, 27galong, 27ga-short, 30ga-short, 30ga-x-short (x-short n= 1/2 in, short = 1 in, long = 13/8 in). Their major advantage is the ability nto perform controlled aspiration during LA injection.

Lidocaine/epinephrine The most commonly used npreparation (2% lidocaine 1:100,000 epinephrine), it gives effective pulpal nanesthesia for 1.5 h and altered soft-tissue sensation for up to 3 h. It is nextremely safe; the maximum dose (adult) is 7 mg/kg or up to 500 mg (13 × n1.8 ml cartridges). It is also available in ampules 1% + 2% lidocaine plain or n1:200,000 epinephrine. There are theoretical criticisms that the maximum dose nis too high, but these have not been borne out in practice.

Prilocaine Similar but of slightly less nduration and effect than that of lido-ocaine/epinephrine. It is available as 4% nprilocaine plain or 4% prilocaine 1:200,000 epinephrine. It may cause nmethemoglobinemia in excess. The maximum safe dose (adult) is 8 mg/kg or up to n500 mg (8 × 1.8 ml cartridges). In reality, there are few hard nindications for the use of prilocaine over lidocaine.

Mepivacaine Available in two forms, 2% with nlevonordefrin 1:20,000 and 3% plain. Short-acting LA is advocated for nrestorative work but has not really caught on. The maximum safe dose is 6.6 nmg/kg or up to 400 mg (11 × 1.8 ml cartridges or 7 × 1.8 ml ncartridges, if plain).

Bupivacaine Long-acting LA available as 0.5% nwith 1:100,000 epinephrine (5-7 h), useful as a postoperative analgesic. The nmaximum safe dose is 2 mg/kg up to 200 mg (10 × 1.8 ml cartridges).

Articaine Available as 4% articaine with n1:100,000 epinephrine. The maximum dose is 7 mg/kg or up to 500 mg in adults, nand 5 mg/kg in children.

Articaine and prilocaine have been reported as nbeing more likely than other anesthetics to be associated with paresthesia. The ndifference was statistically significant when their level of use was taken into naccount.2

Topical anesthetics Lidocaine is the only nreally useful topical anestheic among the above. It is available as a spray or nan ointment applied to mucosa several minutes prior to injecting. There is a nhigh incidence of contact eczema in people frequently exposed to these npreparations, so do not apply with bare fingers. Benzocaine in lozenge or paste nform is used for mucosal anesthesia. Cocaine 4% solution is used as a nasal nmucosal anesthetic and vasoconstrictor.

 

A mix of lidocaine and prilocaine is an invaluable nskin topical analgesic, used prior to venepuncture in children.

Handling equipment Use one cartridge and nneedle per patient. Discard cartridge if a precipitant is seen in the solutioor if air bubbles are present. Store in a cool, dark place and use before nexpiration date. Warm cartridge to reduce discomfort and load into the syringe nimmediately prior to use. Aspirate before injecting. The ↑ risk nassociated with needlestick injuries has spawned a number of devices to aid isafely recapping needles. The Centers for Disease Control and U.S. Department nof Labor Occupational Safety and Health Administration (OSHA) have beeconcerned about the potential risk for disease transmission presented by the nrecapping of needles. OSHA requires that health-care facilities (including ndental offices) continually evaluate and consider the uses of new devices ndeveloped to address this concern.

 

Local anesthesia—techniques

The inferior alveolar dental block and local ninfiltrations are the mainstay of LA technique; however, numerous others are navailable as alternatives, supplements, and fallbacks.

  IAB n(inferior alveolar block) Technique of choice for mandibular molars; also neffective for mandibular premolars, canines, and incisors (the latter if nsupplemented by infiltration). The aim is to deposit solution around the ninferior alveolar nerve as it enters the mandibular foramen underneath the nlingula. The patient’s mouth must be wide open. Palpate the landmarks of nexternal and internal oblique ridges and note the line of the nptyerygomandibular raphe. With the palpating thumb lying in the retromolar nfossa, insert the needle at the midpoint of the tip of the thumb slightly above nthe occlusal plane lateral to the ptyerygomandibular raphe. The needle is ninserted ~0.5 cm and if a lingual nerve block is required, 0.5 ml of LA is ninjected at this point. The syringe is then moved horizontally ~40° across the ndorsum of the tongue and advanced to make contact with the lingula. Once bony ncontact is made, the needle is withdrawn slightly and the remainder of the LA ninjected. It should never be necessary to insert the needle up to the hub. Note nthat the mandibular foramen varies in position with age (for children, see p. n78). In the edentulous, the foramen, and hence the point of needle insertion, nis relatively higher than in the dentate.

Gow-Gates technique Blocks sensation in Vc by ndepositing LA at head of condyle.1 Akinosi approach: LA is deposited above the nlingua.2

 Long nbuccal block The long buccal nerve is anesthetized by injecting 0.5-1 ml of LA nposterior and buccal to the last molar tooth.

 Mental nnerve block The mental nerve emerges from the mental foramen lying apical to nand between the first and second mandibular premolars. LA injected in this nregion will diffuse in through the mental foramen and provide limited nanesthesia of premolars and canine and, to a lesser degree, incisors on that nside. It will provide effective soft-tissue anesthesia. Place the lip otension and insert the needle parallel to the long axis of the premolars nangling toward bone, and deposit the LA. Do not attempt to inject into the nmental foramen as this may traumatize the nerve. LA can be encouraged in by nmassage.

 Sublingual nerve block An anterior extensioof the lingual nerve can be blocked by placing the needle just submucosally nlingual to the premolars; use 0.5 ml of LA.

Posterior superior alveolar block Ainfrequently indicated technique. The needle is inserted distal to the upper nsecond molar and advanced inward, backward, and upward close to bone for ~2 cm. nLA is deposited high above the tuberosity after aspirating to avoid the nptyerygoid plexus.

Nasopalatine block Profound anesthesia can be nachieved by passing the needle through the incisive papilla and injecting a nsmall amount of solution. This is extremely painful (for hints on how to novercome pain on palatal injections see below).

 Infraorbital block Rarely indicated. Palpate nthe inferior margin of the orbit as the infraorbital foramen lies ~1 cm below nthe deepest point of the orbital margin. Hold the index finger at this point nwhile the upper lip is lifted with the thumb. Inject in the depth of the buccal nsulcus toward your finger, avoid your finger, and deposit LA around the ninfraorbital nerve.

 Infiltrations The aim is to deposit LA nsupraperiosteally in as close proximity as possible to the apex of the tooth to nbe anesthetized. The LA will diffuse through periosteum and bone to bathe the nnerves entering the apex. Reflect the lip or cheek to place mucosa on tensioand insert the needle along the long axis of the tooth aiming toward bone. At nthe approximate apex of tooth, withdraw slightly and deposit LA slowly. For npalatal infiltrations, achieve buccal anesthesia first and infiltrate ninterdental papillae; then penetrate palatal mucosa and deposit small amount of nLA under force.

Intraligamentary anesthesia Individual teeth ncan be rendered pain-free by injecting small amounts of LA along the nperiodontal membrane via a specially designed system (high-pressure syringe and nultra-fine needles). This has the advantage of rapid onset and specific nanesthesia to isolated teeth; it is a useful adjunct to conventional LA and isome hands may replace it for minor procedures. Disadvantages include npost-injection discomfort due to temporary extrusion and an apparent ↑ nincidence in dry socket.

Electronic dental anesthesia (EDA) Aaggressively marketed technique based on the principles of transcutaneous nelectric nerve stimulation (TENS). Uses electrodes, buccally and lingually, nwhich carry a minute electrical current to interfere with local nerve nconduction and hence pain appreciation. This technique may be of value irestorative procedures and others not requiring the profound anesthesia or nvasoconstrictive effects of LA.

Intraosseous anesthesia A recently nreintroduced technique that produces profound single-tooth anesthesia. nSpecialized equipment and technique are needed (e.g., Stabident System, Fairfax nDental; X-Tip, Dentsply). The procedure involves choosing a suitable site for a nlateral perforation of the alveolar bone. A site distal to the area to be nanesthetized, approximately 2 mm apical to the gingival margin between the nroots of the teeth, is ideal. The soft tissue of the perforation site is ninfiltrated with a small dose of LA. A bone perforator is then used in a ncontra-angle handpiece to perforate the cortical bone. A short needle is used nto slowly deposit LA into the bone perforation.

•          ▶ When developing LA technique there is no alternative to seeing, ndoing, and doing again.

Local anesthesia—problems and hints

Failure of anesthesia

There are enormous differences in individual nresponse to a standard dose of LA—in the speed of onset, duration of action, nand the depth. Soft-tissue anesthesia is more easily obtained, needing a lower ndegree of penetration of solution into nerve bundles than anesthesia from npulpal stimulation. A numb lip does not ∴ indicate pulpal anesthesia.

Causes of failure include the following:

•          Poor ntechnique and inadequate volume of LA

•          Injectiointo a muscle (will result in trismus, which resolves spontaneously).

•          Injectiointo an infected area (which should not be done anyway as this risks spreading nthe infection)

•          Intravascular ninjection; clearly of no anesthetic benefit. Small amounts of intravascular LA ncause few problems. For toxicity, see p. 510.

•          Dense ncompact bone can prevent a properly given infiltration from working. Counter by nusing intraligamentary, intraosseous, or regional LA.

•          Infrequently, nanastomosis from either aberrant or normal nerve fibers not transmitted with a nblocked nerve bundle

Pain on injection

This is to a certain degree inevitable, but ncan be ↓ by patient relaxation; application of topical LA; stretching the nmucosa; and slow, skilful, accurate injection of slightly warmed solution ireasonable quantities. Causes of pain include the following:

•          Touching nthe nerve when giving blocks, resulting in “electric shock” sensation and nfollowed by rapid anesthesia (it is extremely rare for any permanent damage to noccur)

•          Injectioof contaminated solutions (particularly by copper ions from a preloaded ncartridge). Avoid by loading the cartridge immediately prior to use.

•          Subperiosteal ninjections are painful and unnecessary, ∴ avoid.

Other problems with administration

Lacerated artery May be followed by an area of nischemia in the region supplied, or painful hematoma. Rare.

Lacerated vein Followed by a hematoma, which nresolves fairly quickly.

Facial palsy Can be caused by incorrect distal nplacement of the needle tip, allowing LA to permeate the parotid gland. The npalsy lasts for the duration of the LA.

Post-injection problems

Lip and cheek trauma Tell patient to avoid nsmoking, drinking hot liquids, and biting lip or cheek. Assure them that the nsensation will pass in a few hours and that their face is not swollen (whether nadult or child). If the advice goes unheeded and they return with traumatized nmucosa, treat with antiseptics or antibiotics and simple anesthesia.

Needle-tract infection Rare. Use nbroad-spectrum antibiotic if needed.

 

General points

Thick nerve trunks require more time for npenetration of solution and more volume of LA. Ierve trunks autonomic nfunctions are blocked first, then sensitivity to temperature, followed by pain, ntouch, pressure, and motor function. Concentration of anesthesia ↑ nrapidly around the nerve at first and provides soft tissue anesthesia; however, nthis is reached substantially before the levels needed for pulpal anesthesia, nwhich takes several minutes and will wear off first (usually within an hour of na standard lidocaine/epinephrine LA). Disinfection of mucosa prior to LA is not nrequired; however, sterile disposable needles are absolutely mandatory because nof risks of cross-infection.

Sedation—nitrous oxide-oxygen

Nitrous oxide-oxygen sedation is the most ncommonly used and safest form of sedation in dentistry. It has two aspects: 1 nthe delivery of a mixture of nitrous oxide and O2, and 2 a semi-hypnotic patter nfrom the doctor administering the sedation. In dentistry, two different ntechniques of nitrous oxide sedation have been described: 1 inhalational nsedation with a fixed concentration of nitrous oxide, and 2 titrating nitrous noxide to the patient. In our view the titration technique is the most useful none.

Nitrous oxide

Nitrous oxide has both sedative and analgesic nproperties; the former is the most useful. The analgesic effect requires high nlevels of nitrous oxide. It is an inert gas that does not enter any of the nbody’s metabolic pathways and is distributed as a poorly soluble solution. This nallows very rapid distribution; peak saturation is reached within 5 min and is nsimilarly eliminated (90% in 10 min).

Indications It is of particular value ianxious patients undergoing relatively atraumatic procedures and in children, nfor whom the benzodiazepines are less suitable.

Contraindications There are few, but upper nairway obstruction, e.g., a cold, is one. First-trimester pregnancy makes the nprocedure difficult and preexisting vitamin B12 deficiency would C/I its use. nOther C/I, e.g., complex medical history, are relative and may limit nitrous noxide use in a dental practice but not in the hospital.

Nitrous oxide pollution This is the major nproblem associated with nitrous oxide use. It is essential to have a scavenging nsystem in place as nitrous oxide accumulation can lead to B12 deficiency and ndemyelination syndromes. There is a real potential hazard to pregnant staff nworking in confined conditions with this gas.

Aim

The goal is to produce a comfortable, relaxed, nawake patient who is able to open their mouth on request with no loss of nconsciousness or the laryngeal reflex. During the procedure, patients will nexperience general relaxation and a tingling sensation often in the fingers or ntoes, and describe feeling mildly drunk. There is often a sense of detachment nand distortion of the sense of time. Rarely, patients may dream despite being nawake, and these can be sexual fantasies, which is another reason for always having na second person in the room at all times.

Technique

A nitrous oxide machine will not deliver less nthan 30% O2. Start by delivering 100% O2 via a nasal mask and set flow control nto match their tidal volume (flow rates 6-8 1/min for adult, 4 1/min for child). nThen give 10% nitrous oxide for 1 min, ↑ (if needed) to 20% for 1 min, n↑ to 30% (if needed) for 1 min, and so on. Most patients achieve adequate nlevels of sedation at 20-30%; some may require less, a few a bit more. Remember nthat nitrous sedation relies on the reassuring banter of the operator more thaany of the other sedation technique, and many view this as hypnosedation. Give nLA and carry out Rx. To discontinue, turn flow to 100% O2 and oxygenate patient nfor 5 min. Then remove mask and get the patient to sit in a recovery room for n10 min, by which time 90% of the nitrous oxide will have been blown off and nthey will be safe to leave the operating room.

Sedation—benzodiazepines

General pointers, problems, and hints

Benzodiazepines are both sedative and hypnotic ndrugs useful for sedation of patients. Two techniques are generally used: oral nand IV.

Elderly patients tend to be very sensitive to nbenzodiazepines and doses are best halved in the >60 age group initially. nInterestingly, children show not only resistance to these drugs but sometimes nparadoxical stimulation, and benzodiazepine sedation is not recommended for nthose <16 years.

Postoperative drowsiness is perhaps the nbiggest problem, as patients may be influenced by, e.g., diazepam, for up to 24 nh after administration (this time is ↓ with midazolam). There is also a nre-sedation effect caused by enterohepatic recirculation.

IV sedation This is the most efficient and neffective method of extending the use of LA in dental Rx; however, it requires nsubstantial skill and confidence in venepuncture and administration of the ndrugs; ∴ an inexperienced operator and a patient with nneedle phobia form relative C/I, as do inability to be accompanied, the need to nbe in a responsible position within 24 h of sedation (e.g., looking after young nchildren on one’s own, driving, etc.), patients with liver or renal impairment, nglaucoma, psychoses, pregnancy, or a demonstrated allergy to the nbenzodiazepines.

Certain drugs interact, including cimetidine, ndisulfiram, anti-parkinsonian drugs, other sedatives, narcotic analgesics, nantiepileptic drugs, antihistamines, and antihypertensives. Patients on these nmay be best treated (and then cautiously) in a hospital environment. Patients naddicted to alcohol or other drugs may require a substantial dose modification, nusually a big ↑. Those being sedated need to give written informed nconsent. Always provide written postoperative instructions because patients nwill not remember verbal ones. The role of the doctor administering sedation is nsupported by a second appropriate person, i.e., one trained in CPR, who must be npresent. At no time should the patient lose consciousness during IV sedation. nThe addition of any drug, especially opioids, converts a technique with a wide nsafety margin into one with a very narrow margin and confers no routine nadvantage.

Multiple drug techniques should be used by ntrained anesthesiologists. There is no need to starve patients prior to being nsedated, although many local policies dictate this and oral medication should nbe continued. Rectal sedation is popular in some countries, using a prepackaged nsolution of diazepam given PR dose 2-10 mg.

Flumazenil A specific benzodiazepine reversal nagent. Dose: 200 µg IV over 15 sec followed by 100 µg at 60-sec intervals until nreversal occurs. Note: This drug has a shorter half-life than the drugs it will nreverse, ∴ nmultiple doses may be required. Patients should never be reversed, then left nunsupervised. This is an essential emergency drug for IV sedation.

Benzodiazepines—techniques

Oral sedation

This is of use for managing moderately anxious npatients. There are problems, however, with absorption time and the risk of nsedation occurring too early or too late. There is again a risk of patients nhaving sexual fantasies under the influence of these drugs. Two drugs are used:

Temazepam 30 mg, 1 h pre-Rx produces a degree nof sedation similar to that seen with IV techniques.

Diazepam, either divided regimen, 5 mg night nbefore, 5 mg morning of Rx, and 5 mg 1 h pre-Rx; or as 10-15 mg 1 h prior to nRx. Both drug and technique are highly variable in consistency and quality of nsedation achieved. Both doses may have to be modified depending on the size and nage of the patient.

IV techniques

A far greater control of the duration and ndepth of sedation can be consistently achieved with this approach. It gives nexcellent sedation with detachment for ~30 min with amnesia for the duration of nRx. The major disadvantage is a potential for respiratory depression, post-Rx ndrowsiness, and amnesia (a reversal agent is available but not suitable for nroutine reversal of conventional sedation, see p. 580). Skill with venepuncture nis a prerequisite of the technique. Diazepam has been entirely superseded by ndiazepam in lipid emulsion (diazemuls) as diazepam is not water-soluble and is nvery irritant.

Midazolam A water-soluble benzodiazepine of nroughly double the strength of diazepam. It has a much shorter half-life, with nno significant metabolites, creating a quicker and smoother recovery, and it is nmore amnesic than diazepam. It is supplied in both 2 ml and 5 ml ampoules, both ncontaining 10 mg midazolam (5 ml ampoule is preferable, as it is easier to ncontrol the increments, given at 1 mg/increment). It is the drug of choice.

Diazepam Diazepam is metabolized to desmethyldiazepam, nwhich has a long half-life. It is presented in an ampoule containing 10 mg ndiazepam, given in slow IV increments (usually 2.5 mg via a butterfly) until nsigns of sedation are observed. The suggested maximum dose is 20 mg.

IV technique

Relax the patient and have them sitting in the nchair. Place a tourniquet around the most convenient arm and ask them to dangle nthe arm at their side. Any useful veins on the dorsum of the hand will become nquickly evident. While this is happening, get your equipment ready: sticky ntape, spirit wipe, butterfly, and drug in syringe. Look at the hand; is there a nreasonable straight segment of vein? (If not, cut your losses and look nelsewhere.) If there is, secure the hand with your nondominant hand, palmar nsurface to palmar surface, with your thumb in a position to tense the skioverlying the selected vein. Stroke the back of the hand and tap the vein to nengorge it. Prepare the skin with alcohol wipe; get your assistant to help nremove the needle cover and inform the patient there will be a slight scratch. nIntroduce the butterfly tip at a shallow angle through skin, then ↓ the nangle further and move along the line of the vein until it has entered, as nrevealed by a flashback into the extension tubing. Then introduce the length of nthe needle along the vein carefully, so as to avoid cutting through, and secure nwith tape. Remove air by aspirating blood into the tubing and release ntourniquet. Place the patient in the supine position and give a small bolus n(2-3 mg diazepam, 1-2 mg midazolam). Wait for 1 min and then give further nincrements until an adequate level of sedation is achieved. Leave the butterfly nin to maintain venous access. Loss of laryngeal reflex constitutes oversedatioand means you must stop and ensure that the airway is patent, only proceeding nif there is no respiratory depression and the airway can be protected.

Monitoring A second appropriate person must be npresent. Pulse and BP should be monitored. Pulse oximetry is mandatory. Aitchy nose is an early sign of “complete” sedation. Hiccups constitute noversedation.

Post-sedation Allow time for recovery (30-60 nmin) in calm surroundings. The patient must be accompanied home and forbiddeto drive or assume a responsible position for 24 h.

Anesthesia—drugs and definitions

Sedation is a triad of depressed nconsciousness, muscle relaxation, and analgesia.

IV anesthetic agents

Thiopental (dose 4 mg/kg) Although aultra-short-acting barbiturate anesthetic, its half-life is 6-12 h. It is a npoor analgesic and relatively sparing to the laryngeal reflexes, requiring a ngreater depth of anesthesia to prevent laryngospasm. It is highly irritant oinjection but cheap and very popular as an inpatient induction agent. It will nabolish epileptic seizures in induction doses.

Propofol (dose 2.5 mg/kg) A true nultra-short-acting anesthetic as it is completely metabolized within minutes. nIt is less irritant than the others and is the drug of choice for day-case nanesthesia.

Etomidate (dose 0.3 mg/kg) An IV inductioagent often used for patients with compromised cardiovascular systems. It cabe associated with involuntary movements, cough, and hiccup. Avoid itraumatized patients.

Ketamine (dose 1-2 mg/kg) Can be given IM at nhigher doses (unique among anesthetic agents for this). It tends to maintaithe airway and causes little respiratory depression. Its use is limited by a nhigh incidence of severe nightmare hallucinations in adults, which are eased by nmidazolam.

Inhalational anesthetics

Nitrous oxide An excellent analgesic but weak anesthetic, nmainly used to supplement other inhalational anesthetics or in RA. A problem is ncreated by its rapid excretion if used for perianesthetic analgesia; it wears noff rapidly, so it has no postoperative analgesic benefits.

Halothane Largely superseded by newer agents, nit is a weak analgesic, causing hypotension and dysrythmias. The concomitant nuse of injected epinephrine should be avoided ion-ventilated patients nbreathing halothane as it ↑ risk of ventricular fibrillation (VF). It is nvery rarely hepatotoxic after repeated anesthetics in adults, and extremely nrarely used de novo.

Enflurane A weaker anesthetic than halothane nbut less likely to produce dysrythmias or hepatitis. Avoid in epileptics.

Sevoflurane A newer agent with rapid onset and nrecovery. It is good for inhalation induction and has become increasingly the ninhalational agent of choice.

All inhalational agents cause muscle nrelaxation.

Muscle relaxants

These are used to create laryngeal relaxatiofor intubation; this stops patients breathing, and they must then be ventilated nuntil the agent wears off or is reversed.

Succinylcholine Used for emergency cases for nrapidly securing airway. It is a short-acting depolarizing muscle relaxant, nwith quick, good recovery but cannot be reversed. The main problems for the npatient are muscle pains, which arise 24-48 h after administration. These cabe very severe and are more likely in the ambulant. It can also cause severe nbradycardia, especially on a repeat dose in children. It is metabolized by plasma ncholinestese, absence of which can lead to succinylcholine sensitivity (p. n488). It causes an ↑ in K+, ∴ know U&Es in all but very routine cases.

Pancuronium, atracurium, vecuronium, and nrocuronium All non-depolarizing muscle relaxants; slower acting and longer nlasting, but can be reversed using neostigmine.

Analgesics Opioids are mainstay, and include nthe following:

•          Morphine; nlong acting, mainly used for postoperative analgesia

•          Fentanyl; nfirst of the short-acting opioids

•          Alfentanil; npurely used as anesthetic opioid due to short duration

•          Remifentanil; ncontinuous infusioeeded because of ultra-short duration; ideal as anesthesia nadjunct but not postoperative pain relief

Anesthesia and the patient on medication

Certain drugs should ring alarm bells whepatients require a GA. These include the following:

Monoamine oxidase inhibitors Should be stopped n2 weeks prior to GA.

Antiepileptic drugs Must be continued up to, nduring, and after GA; however, methohexitone should be avoided.

Antihypertensives Should be continued, but nensure that the anesthesiologist is aware they are being taken.

Bronchodilators Should be continued. Give ninhaler with premedication and ensure that nebulizer is available npostoperatively.

Cardioactive drugs Should all be continued. Warthe anesthesiologist, as these patients often benefit from a preoperative nanesthetic assessment.

Cytotoxics Patients on these rarely need GA, nbut if they do, they need FBC, U&Es, and LFTs. Suxamethonium should be navoided.

Diabetic drugs For management, see p. 530.

Lithium Measure levels. Omit prior to major nsurgery.

Oral contraceptives Think about DVT nprophylaxis, although experience suggests the risk is remote. The NIH nrecommends discontinuing 4 weeks prior to major elective surgery; this is ngenerally unnecessary for maxillo-facial/oral surgery. Be guided by local npolicy. HRT does not need to be stopped.

Sedatives and tranquillizers If the patient ntakes a regular dose these can be maintained, but warn the anesthesiologist.

Corticosteroids Patients on long-term steroids nrequire supplementation; see p. 488, 512, 531.

Oral anticoagulants Stop and heparinize for nall major surgery. Monitor clothing. Monitor INR for warfarin.

Anesthesia—hospital setting

With the exception of the outpatient GA nservice provided by dental hospitals, GA in a hospital setting is similar to nthat for any other surgical service. The provision for and the care of the npatient immediately prior to, during, and after the anesthetic is the domain of nthe trained anesthesiologist. The input from the hospital junior staff is the nsame, whether in a dental or surgical specialty, and is mainly covered on p. n518. The fundamental problem for any dental, oral, or maxillofacial anesthetic nis that the surgeon and anesthesiologist both need to have access to the same nanatomical site: the shared airway. The means by which this is overcome ihospital practice is by endotracheal, particularly nasendotrachea, intubation, nmuscle relaxation, and ventilation.

Endotracheal intubation secures the airway by nplacing a tube into the trachea via the nose, mouth, or a tracheostomy. This ntube has an inflatable cuff that prevents aspiration of debris and is connected nto an anesthetic machine to allow delivery of O2, nitrous oxide, and ainhalational anesthetic. Most anesthesiologists also use a throat pack to nsupplement the cuff, which must be removed at the end of the operation. nIntubation is a specialist skill and must be learned with practice; skilled npractitioners can perform blind nasendotracheal intubation, which is of nenormous value in cases with trismus; most cases are, however, performed by ndirect vision of the vocal cords using a laryngoscope with the patient’s neck nfully extended. The major risk of intubation is intubating the esophagus and nnot recognizing it. Other complications include: traumatizing teeth; vocal cord ngranulomata; minor trauma to the adenoids; rarely, pressure necrosis of ntracheal mucosa; and laryngeal stenosis.

The laryngeal mask airway (LMA) The LMA has nbecome an acceptable method of maintaining the airway. Structurally, it is a ncurved tube with a large cuff at its end. It is a device inserted orally nwithout direct vision following the normal curve of the pharynx. Its onward nprogression is stopped by the upper end of the esophagus and at this point the ncuff is inflated, forming a seal around the entrance to the larynx. Patients nmust be starved as it does not protect against aspiration. It occupies a nsubstantial volume in the mouth. The necessity of movement of the LMA to allow nsurgical access may displace the cuff, possibly causing laryngeal obstruction. nThe LMA is expensive, but autoclavable up to 40 times. Quite deep anesthesia is nrequired to both pass and maintain the LMA, which may prolong anesthesia ninappropriately. The LMA should only be used by those trained in intubation.

Muscle relaxation Essential for successful nintubation in elective patients. These drugs are covered on p. 585. For most noral surgery, once the patient is intubated, ventilation is aided by small ndoses of non-depolarizing muscle relaxant. An alternative is a continuous ninfusion of a very shortacting opioid (e.g., remifentanil).

Ventilation May be hand or mechanical. The nlatter is more precise and convenient for the anesthesiologist. It involves a nmachine providing intermittent +ve pressure ventilation.

Monitoring There are increasingly nsophisticated noninvasive techniques available: pulse oximetry to measure the npercutaneous saturation of hemoglobin with O2 (a normal person breathing air nwill have a saturation >95%); capnograph to measure end-tidal PetCO2 n(normal: 5.2 kPa or 40 mmHg); ECG and automatic BP machines. It must be nstressed, however, that these machines do not replace, only ↑, the nability of the anesthesiologist to use clinical observation of pulse, color, nskin changes, and ventilatory pattern. The minimum standard of monitoring is nBP, ECG, SaO2, and end-tidal CO2. Patient safety standards, guidelines, and nquality assurance measures for the administration of anesthesia in the United nStates have been developed by the American Society of Anesthesiologists.

Malignant hyperthermia

Anesthesia—practice setting

The ideal team to provide exodontia under GA nis a small, skilled group, e.g., anesthesiologist, dentist, and nurse, who have nreceived appropriate postgraduate training and have suitable facilities.

Outpatient anesthesia is given to healthy npatients; most anesthetics, from induction to recovery, are a few minutes.

Controversial points

Pollution with anesthetic gases In the nhospital environment it is possible to scavenge the majority of gases as npatients are either intubated or have an LMA or a relatively leak-proof face nmask. This is not the case in dental surgery, as patients are breathing through na nasal mask and, invariably, through their mouths.

Hazards of inhaling anesthetic gases These are nnot well established. It is true that patients continuously breathing nitrous noxide for 24 h or so begin to have suppression of the bone marrow and that nchronic recreational abuse can cause subacute combined degeneration of the nspinal cord. The short-term and intermittent long-term effects of exposure to nnitrous oxide, halothane, enflurane are, however, simply not known. It remains ncommon sense that no one should work in a polluted atmosphere. OHSA sets nstandards to ensure that health-care workers are not exposed to any unnecessary nrisks to their health and safety while in the workplace.