SYSTEMIC COMPLICATIONS.pdf

312 PART IV Complications, Legal Considerations, Questions, and the Future • Fig. 17.6 Surgical excision of needle fragment (see the patient from Fig. 17.5). (Courtesy Dr. Carlos Elias De Freitas CVM. From Malamed SF, Reed KR, Poorsattar S. Needle breakage: incidence and prevention. Dent Clin N A...

312 PART IV Complications, Legal Considerations, Questions, and the Future • Fig. 17.6 Surgical excision of needle fragment (see the patient from Fig. 17.5). (Courtesy Dr. Carlos Elias De Freitas CVM. From Malamed SF, Reed KR, Poorsattar S. Needle breakage: incidence and prevention. Dent Clin N Am. 2010;54:745–756.) an “electric shock” or “zap” throughout the distribution of the involved nerve as the injection is being administered. Although it is exceedingly difficult (and highly unlikely) to actually sever a nerve trunk or even its fibers with the small needles used in dentistry, trauma to a nerve produced by contact with the needle is all that may be needed to produce paresthesia.33,34 Insertion of a needle into a foramen, as in the second division (maxillary) nerve block via the greater palatine foramen, also increases the likelihood of nerve injury. Hemorrhage into or around the neural sheath is another cause. Bleeding increases pressure on the nerve, leading to paresthesia.32-34,36 Edema following surgical procedures is another potential cause of paresthesia, as the pressure of the edematous fluid compresses the nerve. The local anesthetic solution itself may contribute to the development of paresthesia after local anesthetic injection.40 Haas and Lennon32 took a retrospective look at paresthesia after injection of local anesthetic in dentistry in the province of Ontario, Canada, over a 20-year period (1973 to 1993). Their report included voluntary submissions by dentists to their insurance carriers for claims of paresthesia. Only cases where no surgery was performed were considered. One hundred forty-three cases of paresthesia unrelated to surgery were reported in this period. All reported cases involved the inferior alveolar nerve or the lingual nerve or both, with anesthesia of the tongue reported most often, followed by anesthesia of the lip. Pain (hyperesthesia) was reported by 22% of patients. Paresthesia was reported more often after administration of a 4% local anesthetic—prilocaine hydrochloride and articaine hydrochloride. Observed frequencies of paresthesia after administration of articaine hydrochloride and prilocaine hydrochloride were greater than expected, based on the distribution of local anesthetic use in Ontario in 1993.32 According to Haas and Lennon32 the incidence of paresthesia resulting from all local anesthetics is approximately 1 in 785,000; for 0.5%, 2%, and 3% local anesthetics, it is approximately 1 in 1,250,000; and for 4% local anesthetics, it is approximately 1 in 485,000. In 2006 Hillerup and Jensen41 in Denmark, reviewing insurance claims, suggested that articaine should not be used for IANB because it had, in their opinion, a greater propensity for paresthesia. Yet, of the 54 case reports of paresthesia reviewed, 42 (77%) involved not the inferior alveolar nerve but the lingual nerve (see later discussion) (Table 17.2). In response to Hillerup and Jensen’s article, the Pharmacovigilance Working Committee of the European Union reviewed reports of paresthesia associated with articaine and other local anesthetics in 57 countries, estimating that the number of patients treated with articaine is approximately 100 million annually.42 Their published report (October 30, 2006) states the following: “This investigation is a followup to an inquiry initiated in 2005. This enquiry resulted from suspicions that were raised in Denmark, that a local anesthetic, articaine, was responsible for an increased risk of nerve injuries compared with the risk associated with other local anesthetics (mepivacaine, prilocaine, lidocaine).” The report concluded: “Regarding articaine, the conclusion is that [the] safety profile of the drug has not significantly evolved since its initial launch (1999 in Denmark). Thus, no medical evidence exists to prohibit the use of articaine according to the current guidelines listed in the summary of product characteristics.”42 “All local anesthetics may cause nerve injury (they are neurotoxins). The occurrence of sensory impairment is apparently slightly more frequent following use of articaine and prilocaine. However, considering the number of patients treated, sensory impairments rarely occur. For example, the incidence of sensory impairment following the use of articaine is estimated to be 1 case in 4.6 million treated patients.” Further they report, “Nerve injuries may result from several incidents: mechanical injury because of needle insertion; direct toxicity from the drug; and neural ischaemia.”42 In 2007 Pogrel43 reported the first clinical evaluation of cases of paresthesia in nonsurgical cases. Evaluation of 57 cases of paresthesia following local anesthetic administration CHAPTER 17 Local Complications 313 TABLE Distribution of Analgesic Solution and Nerve Affected, Including 54 Nerve Injuries in 52 Patients 17.2 Inferior Alveolar Nerve Lingual Nerve Articaine (4%) 5 24 29 (54%) Prilocaine (3%) 4 6 10 (19%) Lidocaine (2%) 3 7 10 (19%) Mepivacaine (3%) 0 4 4 (7%) Mepivacaine (3%) + articaine (4%) 0 1 1 (2%) 12 42 54 (100%) Number of nerve injuries Sum From Hillerup S, Jensen R. Nerve injury caused by mandibular block analgesia. Int J Oral Maxillofac Surg. 2006;35:437–443. TABLE Summary of Incidence of Reported Nerve Injury From 2003 to 2011 17.3 Ratio (1.0 Expected) Anesthetic 200743 201244 Lidocaine hydrochloride 0.64 0.5 Articaine hydrochloride 1.19 0.97 Prilocaine hydrochloride 4.96 2.2 Mepivacaine hydrochloride Not reported 3.25 Modified from Pogrel MA. Permanent nerve damage from inferior alveolar nerve blocks—an update to include articaine. J Calif Dent Assoc. 2007;35:271–273; and Pogrel MA. Permanent nerve damage from inferior alveolar nerve blocks—a current update. J Calif Dent Assoc. 2012;40:795–797. (over a 3-year period, 2003 to 2005) revealed that lidocaine was responsible for 35% of cases, articaine for 29.8%, and prilocaine for 29.8%. He presented the following as the reason for his research and writing of the article: “We were aware of the discussion in dental circles as to the use of articaine for inferior alveolar nerve blocks and are aware of recommendations suggesting that it not be used for IANBs. This was the predominant reason for submitting this paper at this time.”43 In 2012 Pogrel44 reported on an additional 41 patients he evaluated from 2006 through 2011. He concluded: “of the cases referred, it would appear that despite the fact that articaine may be used less for inferior alveolar blocks than it was and used more for infiltrations because of its great penetrating power, it is still causing cases of permanent inferior alveolar and lingual nerve damage, which is proportionate to its market share.”44 All local anesthetics are neurotoxic. If all local anesthetics were equally neurotoxic, then the percentage of reported cases of paresthesia for any given drug should be equal to its percentage of market share. For example, if a drug had a 30% market share, it should then account for 30% of the reported cases of paresthesia—a 1:1 ratio (reported as 1.0). From Pogrel’s statistics,43,44 lidocaine, with 54% market share and 35% of the reported cases of paresthesia, had a ratio of 0.64 in 2007 and 0.5 in 2012—better than expected. Prilocaine, on the other hand, with a 6% market share, had 29.8% of the reported cases—a ratio of 4.96 in 2007) and 3.25 in 2012. Articaine, with 25% market share at the time, had 29.8% of the reported cases—a ratio of 1.19 in 2007 and 0.97 in 2012. Mepivacaine, reported in 2012 had 11% of the reported cases of paresthesia and a ratio of 2.2. Table 17.3 summarizes Pogrel’s two articles.43,44 Pogrel concluded that “using our previous assumption that approximately half of local anesthetic used is for inferior alveolar nerve blocks, then on the figures we have generated from our clinic, we do not see disproportionate nerve involvement for articaine.”43 In his discussion, Pogrel also noted that “many of the reports to outside agencies do not report whether the paresthesia was temporary or permanent, and because it is known that most of the paresthesias are temporary and do eventually recover, only reports of persistent issues for nine months or longer should be considered permanent.”44 In July 2010, Garisto et al.45 reported on the occurrence of paresthesia after dental local anesthetic administration in the United States. Data were gathered from the US Food 314 PART IV Complications, Legal Considerations, Questions, and the Future TABLE Incidences of Paresthesia Reported to the Adverse Event Reporting System From 1997 17.4 to 2008 Anesthetic Incidence Mepivacaine 1 in 623,112,900 Lidocaine 1 in 181,076,673 Bupivacaine 1 in 124,286,050 Overall 1 in 13,800,970 Articaine 1 in 4,159,848 Prilocaine 1 in 2,070,678 Being struck by lightning (annual risk) 1 in 328,000 to 1 in 700,000 Data derived and modified from Garisto GA, Gaffen AS, Lawrence HP, et al. Occurrence of paresthesia after dental local anesthetic administration in the United States. J Am Dent Assoc. 2010;141:836–844. and Drug Administration (FDA) Adverse Event Reporting System (AERS). Over an almost 11-year reporting period (November 1997 to August 2008), 248 cases of paresthesia following dental local anesthesia were reported, of which 94.5% involved IANB. Of the reported cases, 89.0% involved only the lingual nerve. Table 17.4 reports the incidence of paresthesia calculated for each dental local anesthetic. As a comparison, the reported risk of being struck by lightning in a given year in the United States is between 1 in 328,00046 and 1 in 700,000.47 One hundred eight of the 248 cases of paresthesia were reported as having resolved completely over a range of from 1 day to 736 days. Confirmed resolution occurred in 34 of the 108 cases (31.4%). Of these, 25 resolved within 2 months, and the remaining 9 resolved within 240 days.45 However, the report by Garisto et al. relied on data from the AERS. The FDA website for AERS displays the following warning: “AERS data do have limitations. First, there is no certainty that the reported event was actually caused by the product. FDA does not require that a causal relationship between a product and event be proven, and reports do not always contain enough detail to properly evaluate an event. Further, FDA does not receive all adverse event reports that occur with a product. Many factors can influence whether or not an event will be reported, such as the time a product has been marketed and publicity about an event. Therefore, AERS cannot be used to calculate the incidence of an adverse event in the U.S. population.”48 A meta-analysis of the efficacy and safety of articaine versus lidocaine, published in 2010, concluded that “this systematic review supports the argument that articaine as compared with lignocaine provides a higher rate of anesthetic success, with comparable safety to lignocaine when used as infiltration or blocks for routine dental treatments.”49 All Injections Are Blind As of December 2018, although articaine hydrochloride, in most countries, including Canada and the United States, is either the first or second most used dental local anesthetic,50,51 the “controversy” occasionally flares anew. Proponents of one side of the argument adamantly believe that 4% local anesthetics do carry a greater risk of paresthesia, be it transient or permanent, but others believe, as adamantly, that other factors are usually involved, primarily mechanical trauma, especially when the paresthesia involves only the lingual nerve, as is the case in 89% of the cases cited by Garisto et al.45 So, what should the doctor do? As with all procedures under consideration for use by a doctor, as well as with any drugs being considered for administration, the doctor must weigh the benefit to be gained from use of the drug or therapeutic procedure against the risks involved in its use. Only when, in the mind of the treating doctor, the benefit to be gained clearly outweighs its risk should the drug or the procedure be used.␣ Problem Persistent anesthesia, rarely total, in most cases partial, and in most cases transient, can lead to self-inflicted soft tissue injury. Biting or thermal or chemical insult can occur without a patient’s awareness until the process has progressed to a serious degree. When the lingual nerve is involved, the sense of taste (via the chorda tympani nerve) may also be impaired. In some instances, loss of sensation (paresthesia) is not the clinical manifestation of nerve injury. Hyperesthesia (an increased sensitivity to noxious stimuli) and dysesthesia (a painful sensation occurring to usually nonnoxious stimuli) may also be noted. Haas and Lennon32 reported that pain was present in 22% of the 143 cases of paresthesia that they reviewed.␣ Prevention Strict adherence to the injection protocol and proper care and handling of dental cartridges help minimize the risk of paresthesia. Nevertheless, cases of paresthesia will still occur in spite of care taken during the injection. Whenever a needle is inserted into soft tissues, anywhere in the body, in an attempt to deposit a drug (e.g., local anesthetic) as close to a nerve as possible without actually contacting it, it is simply a matter of time before such contact does occur. As Pogrel opined: “It is reasonable to suggest that during a career, each dentist may encounter at least one patient with an inferior alveolar nerve block resulting in permanent nerve involvement. The mechanisms are unknown and there is no known prevention or treatment.”33␣ CHAPTER 17 Local Complications 315 Facial nerve (VII) Temporal branches Zygomatic branches Posterior auricular nerve Buccal branches Cervical branch Parotid salivary gland Mandibular branch • Fig. 17.7 Facial nerve distribution. Management Nichel52 reported that most paresthesias resolve within approximately 8 weeks without treatment.53,54 Only when damage to the nerve is severe will the paresthesia be permanent, and this occurs only rarely. In most situations the degree of paresthesia is minimal, with the patient retaining most of the sensory function to the affected area. Therefore the risk of self-inflicted tissue injury is minimal. Garisto et al.45 in reviewing 248 reports of paresthesia had data on resolution in 108 cases. The period of resolution ranged from as short as 1 day to as long as 736 days. Confirmed resolution of paresthesia was reported in 34 of the 108 cases (31.4%). Of the 34 cases that did resolve, 25 did so within 2 months; the remaining 9 cases resolved within 240 days. In phase 3 clinical trials comparing 4% articaine hydrochloride with epinephrine 1:100,000 (N = 882) with 2% lidocaine with epinephrine 1:100,000 (N = 443), Malamed et al.55 reported the total number of participants who reported these symptoms (paresthesia) 4 to 8 days after the procedure was 8 (1%) for the articaine group and 5 (1%) for the lidocaine group. Although more articaine patients than lidocaine patients were believed by the investigators to have drug-related symptoms, in five cases (four with articaine, one with lidocaine), the symptoms did not begin on the day of study drug administration, suggesting that they were caused by the (dental) procedure rather than the anesthetic. In cases for which resolution dates were available, it was determined that the duration of these events was less than 1 day to 18 days after the procedure. In all cases, the paresthesia ultimately resolved. McCarthy56 and Orr57 have recommended the following time-honored sequence in managing the patient with a persistent sensory deficit after local anesthesia: 1. Be reassuring. The patient usually telephones the office the day after the dental procedure complaining that some area of the mouth is still “numb.” a. Speak with the patient personally. Do not relegate the duty to an auxiliary. Remember that if patients cannot get through to speak to their doctor, they can always get the doctor’s attention through litigation. b. Explain that paresthesia is not uncommon after local anesthetic administration. Sisk et al.58 reported that paresthesia may develop in up to 22% of patients in very select circumstances. c. Arrange an appointment to examine the patient. d. Record the incident in the dental record. Thorough record keeping can be of paramount importance in the event of litigation. 2. Examine the patient in person. a. Determine the degree and extent of paresthesia. b. Explain to the patient that paresthesia normally persists for at least 2 months before resolution begins, and that it may last up to a year or longer. c. “Tincture of time” (e.g., observation) is the recommended treatment, although microneurosurgery might, in some instances, be considered as an option, 316 PART IV Complications, Legal Considerations, Questions, and the Future regarding which Pogrel writes: “Although surgical correction is available in some cases, the results are suboptimal.”59 d. Record all findings in the patient’s record using the patient’s own descriptors, such as “hot,” “cold,” “painful,” “tingling,” “increasing,” “decreasing,” and “staying the same.” e. Suggest that simple observation for 1 to 2 months is recommended, but on that same day offer to send the patient for a second opinion to an oral and maxillofacial surgeon, who will be able to map out the affected area and will be able to perform the surgical repair, if that is deemed necessary. f. If surgical repair is suggested by this first consultant, a second opinion should be obtained from another oral and maxillofacial surgeon. It is generally deemed appropriate to observe the situation for minimally 1 to 2 months before considering the surgical option although Pogrel has stated “the chances of a good result may be better if surgery is performed early after the nerve injury, preferably within 10 weeks.”60 3. Reschedule the patient for examination every 2 months for as long as the sensory deficit persists. 4. Dental treatment may continue—if both the doctor and the patient are comfortable doing so—but administration of local anesthetic into the region of the previously traumatized nerve should be avoided. Alternative local anesthetic techniques should be used if possible. 5. It would be advisable to contact your liability insurance carrier should the paresthesia persist without evident resolution beyond 1 to 2 months.␣ Facial Nerve Paralysis The seventh cranial nerve carries motor impulses to the muscles of facial expression, of the scalp and external ear, and of other structures. Paralysis of some of its terminal branches occurs whenever an infraorbital nerve block is administered, or when maxillary canines are infiltrated. Muscle droop is also observed when, occasionally, motor fibers are anesthetized by inadvertent deposition of local anesthetic into their vicinity. This may occur when anesthetic is introduced into the deep lobe of the parotid gland, through which terminal portions of the facial nerve extend (Fig. 17.7). The facial nerve branches and the muscles they innervate are as follows: 1. temporal branches a. frontalis b. orbicularis oculi c. corrugator supercilii 2. zygomatic branches a. orbicularis oculi 3. buccal branches: supplying the region inferior to the eye and around the mouth a. procerus b. zygomaticus c. levator labii superioris d. buccinator e. orbicularis oris 4. mandibular branch: supplying muscles of the lower lip and chin a. depressor anguli oris b. depressor labii inferioris c. mentalis Cause Transient facial nerve paralysis is commonly caused by the introduction of local anesthetic into the capsule of the parotid gland, which is located at the posterior border of the mandibular ramus, clothed by the medial pterygoid and masseter muscles.36,58,61-63 Directing the needle posteriorly or inadvertently deflecting it in a posterior direction during an IANB, or overinsertion during a Vazirani-Akinosi nerve block, may place the tip of the needle within the body of the parotid gland. If local anesthetic is deposited, transient paralysis can result. The duration of the paralysis will equal that of the soft tissue anesthesia associated with the drug.␣ Problem Loss of motor function to the muscles of facial expression produced by local anesthetic deposition is normally transitory. It lasts no longer than several hours, depending on the local anesthetic formulation used, the volume injected, and proximity to the facial nerve. Usually, minimal or no sensory loss occurs. During this time the patient has unilateral paralysis and is unable to use these muscles (see Fig. 17.8). The primary problem associated with transient facial nerve paralysis is cosmetic: the person’s face appears lopsided. No treatment is known, other than waiting for resolution of the drug’s effect. A secondary problem is that the patient is unable to voluntarily close one eye. The protective lid reflex of the eye is abolished. Winking and blinking become impossible. The cornea, however, does retain its innervation; thus if it is irritated, the corneal reflex is intact, and tears lubricate the eye.␣ Prevention Transient facial nerve paralysis is almost always preventable by adhering to protocol with the IANB and the VaziraniAkinosi nerve block (as described in Chapter 14), although in some situations, branches of the facial nerve may lie close to the site of local anesthetic deposition in the IANB and the Vazirani-Akinosi nerve block. A needle tip that comes in contact with bone (medial aspect of the ramus) before depositing local anesthetic solution essentially precludes the possibility that anesthetic will be deposited into the body of the parotid gland during an IANB. If the needle deflects posteriorly during this nerve block and bone is not contacted, the needle should CHAPTER 17 Local Complications 317 • A B be withdrawn almost entirely from the soft tissues, the barrel of the syringe brought posteriorly (thereby directing the needle tip more anteriorly), and the needle readvanced until it contacts bone. Because no contact is made with bone during the Vazirani-Akinosi nerve block, overinsertion of the needle, either absolute (>25 mm) or relative (25 mm in a smaller patient), should be avoided, if possible.␣ Management Within seconds to minutes after deposition of local anesthetic into the parotid gland, the patient senses weakening of the muscles on the affected side of the face. Sensory anesthesia is not present in this situation. Management includes the following: 1. Reassure the patient. Explain that the situation is transient, lasting several hours, and will resolve without residual effect. Mention that it is produced by the normal action of local anesthetic drugs on the facial nerve, which is a motor nerve to the muscles of facial expression. 2. Contact lenses should be removed until muscular movement returns. 3. An eye patch should be applied to the affected eye until muscle tone returns. If resistance is offered by the patient, advise the patient to manually close the affected eyelid periodically to keep the cornea lubricated. 4. Record the incident in the patient’s record. 5. Although no contraindication is known to reinjecting the patient to achieve mandibular anesthesia, it may be prudent to forego further dental care in the affected quadrant at this appointment.␣ Ocular Complications Following injection, local anesthetics diffuse in all directions along a concentration gradient. For injection in the oral Fig. 17.8 Facial nerve paralysis. Inability to close eyelid (A) and drooping of lip on affected side (patient’s left) (B). TABLE Ocular Complications Associated With 17.5 Intraoral Local Anesthetic Administration Amaurosis Blindness Diplopia (double vision) Endophthalmitis Globe penetration Horner syndrome (blepharoptosis, miosis, anhidrosis, hemifacial flushing, conjunctival injection and enophthalmos) Impaired visual acuity (double vision) Mydriasis (dilation of the pupil)) Ophthalmoplegia (internal or external, partial or total) Ptosis Strabismus (convergent or divergent) From Alamanos C, Raab P, Gamulescu A, Behr M. Ophthalmologic complications after administration of local anesthesia in dentistry: a systematic review. Oral Surg Oral Med Oral Pathol Oral Radiol. 2016;121:e39–e350. cavity our desired goal is for the local anesthetic to diffuse into and block nerve conduction from the site of deposition to the brain. The eyes are located relatively close to the mouth, specifically the maxilla, and the diffusing local anesthetic can, on rare occasion, affect the function of nerves around the eyes, producing ocular complications. Alamanos et al.64 in a systematic review reported on 89 cases of ocular complications associated with intraoral injection of local anesthetics. Reviewing literature from 1954 to 2013, they found 65 case reports and one case series (24 cases) for a total of 89 reports of ocular complications following intraoral dental injections. These ocular complications are listed in Table 17.5. Ninety-two percent of the complications were transient. The time for the resolution of a transient ocular complication was more than 6 hours in 25% of the patients. The remainder of the transient cases resolved spontaneously more quickly. Four 318 PART IV Complications, Legal Considerations, Questions, and the Future of the six patients with permanent complications (8%) developed vision impairment (permanent damage of the optic pathway, e.g., partial blindness) and the other two developed an isolated fixed pupil (iridoplegia) that manifested itself clinically as anisocoria (unequal pupil size). Complete permanent blindness had not been reported in the reviewed data.64 In their review of the anesthetic techniques used, Alamanos et al.64 reported that the GowGates mandibular nerve block was associated with only diplopia, whereas vision impairment was associated more often with IANBs than with PSA nerve blocks. The distribution of ocular complications by arch was 46 following maxillary injection and 42 following mandibular injection. The drug most frequently administered when ocular complications occurred was “by far” lidocaine (also the most used local anesthetic in dentistry). There are reports in the literature of permanent65,66 and transient blindness67,68 occurring subsequent to dental local anesthetic injections. Anatomic Basis of Ocular Complications 1. Diffusion of the anesthetic drug through myofascial spaces or bony openings. Sved et al.69 reported a high incidence of diplopia (35.6%) after second division trigeminal blocks (V2) via the greater palatine canal approach. They assumed that the anesthetic solution diffuses through the inferior orbital fissure to affect the extraocular muscles. Ocular complications following mandibular injections were theorized to be a result of the local anesthetic solution being deposited into the area of the upper cervical or stellate ganglia. 2. Inadvertent intraarterial injection of the local anesthetic. Although felt by this author to be highly improbable—as arteries have muscular walls that respond to stimulation by going into spasm—it has been theorized that the combination of an intra-arterial injection and an anatomic variation of the internal maxillary and middle meningeal arteries may direct the anesthetic solution to the ophthalmic artery and from there to the central retinal artery. The vasoconstrictor could then interrupt the blood supply to the retina, resulting in visual phenomena (phosphenes) or blindness, depending on the duration and the degree of vasoconstriction.70 Alamanos et al.64 posit that an intra-arterial route of the anesthetic solution could cause systemic symptoms, skin and mucosal blanching, sensory deficits, vision loss, and parasympathetic denervation. 3. Inadvertent intravenous injection of the local anesthetic. 4. Direct trauma (“scraping”) of the periarterial sympathetic plexus. Such trauma sets up a sympathetic impulse that travels to the orbit. This impulse may account for the transient irradiating pain that can sometimes be experienced during an injection and for the blanching of the skin or mucosa.␣ Management of Ocular Complications Each case involving an ocular complication following intraoral local anesthetic administration should be evaluated individually.64 It is recommended that consultation with an ophthalmologist be obtained whenever there is uncertainty as to the cause. The data reviewed by Alamanos et al.64 showed that diplopia and strabismus always have a transient character and that 75% of the cases resolve within 6 hours. Therefore in conditions such as convergent strabismus or binocular diplopia, at least until the anesthetic effect resolves, a “wait and observe” approach is recommended; supportive measures, such as patient reassurance and patching of the affected eye, should be undertaken, as monocular vision is devoid of distance-judging capability, making it more dangerous for the patient to operate a motor vehicle.64␣ Trismus Trismus, from the Greek trismos, is defined as a prolonged, tetanic spasm of the jaw muscles by which the normal opening of the mouth is restricted (locked jaw). This designation was originally used only in tetanus, but because an inability to open the mouth may be seen in a variety of other conditions, the term is currently used in restricted jaw movement, regardless of the cause.71 Although postinjection pain is the most common local complication of local anesthesia, trismus can become one of the more chronic and complicated problems to manage.72-74 Causes Trauma to muscles or blood vessels in the infratemporal fossa is the most common causative factor in trismus associated with dental injection of local anesthetics. Local anesthetic solutions into which alcohol or cold sterilizing solutions have diffused produce irritation of tissues (e.g., muscle), potentially leading to trismus. Local anesthetics have been demonstrated to be slightly myotoxic to skeletal muscles, especially considering the highly acidic pH of solutions containing a vasoconstrictor (pH ∼3.5 to 4.4). The injection of local anesthetic solution intramuscularly or supramuscularly leads to a rapidly progressive necrosis of exposed muscle fibers.75-77 Hemorrhage is another cause of trismus. Large volumes of extravascular blood can produce tissue irritation, leading to muscle dysfunction as the blood is slowly resorbed (over approximately 2 weeks). Low-grade infection after injection can also cause trismus.78 Every needle insertion produces some damage to the tissue through which it passes. It stands to reason, then, that multiple needle penetrations correlate with a greater incidence of postinjection trismus. In addition, Stacy and Hajjar79 found that of 100 needles used for the administration of IANB, 60% were barbed on removal from the tissues. The barb occurred when the needle came into contact with the medial aspect of the mandibular ramus. CHAPTER 17 Withdrawal of the needle from tissue increased the likelihood of involvement of the lingual or inferior alveolar nerve (e.g., paresthesia) and the development of trismus. Excessive volumes of local anesthetic solution deposited into a restricted area produce distention of tissues, which may lead to postinjection trismus. This is more common after multiple missed IANBs.␣ Problem Although the limitation of movement associated with postinjection trismus is usually minor, it is possible for much more severe limitation to develop. The average interincisal opening in cases of trismus is 13.7 mm (range, 5 to 23 mm).76 The average normal interincisal opening for males is 44.8 (±9.4) mm and for females is 39.2 (±10.8) mm.80 Stone and Kaban81 reported four cases of severe trismus after multiple IANBs or PSA nerve blocks, three of which required surgical intervention. Before surgery, patients had limited mandibular openings of approximately 2 mm, despite usual treatment regimens. In the acute phase of trismus, pain produced by hemorrhage leads to muscle spasm and limitation of movement.82,83 The second, or chronic, phase usually develops if treatment is not begun. Chronic hypomobility occurs secondary to organization of the hematoma, with subsequent fibrosis and scar contracture.84 Infection may produce hypomobility through increased pain, increased tissue reaction (irritation), and scarring.78␣ Prevention 1. Use a sharp, sterile, disposable needle. 2. Properly care for and handle dental local anesthetic cartridges. 3. Use an aseptic technique. Contaminated needles should be changed immediately. 4. Practice the atraumatic insertion and injection technique. 5. Avoid repeated injections and multiple insertions into the same area by gaining knowledge of anatomy and proper technique. Use regional nerve blocks instead of local infiltration (supraperiosteal injection) wherever possible and rational. 6. Use minimum effective volumes of local anesthetic. Refer to specific technique protocols for recommendations. (Chapters 13-15) Trismus is not always preventable.␣ Management In most instances of trismus the patient reports pain and some difficulty opening his or her mouth on the day after dental treatment in which a PSA nerve block or, more commonly, an IANB was administered. Hinton et al.76 reported that the onset of trismus occurred 1 to 6 days after treatment (average, 2.9 days). The degree of discomfort and dysfunction differs but is usually mild. With mild pain and dysfunction, the patient reports minimum difficulty opening his or her mouth. Arrange Local Complications 319 an appointment for examination. In the interim, prescribe heat therapy, warm saline rinses, analgesics, and, if necessary, muscle relaxants to manage the initial phase of muscle spasm.85,86 Heat therapy consists of applying hot, moist towels to the affected area for approximately 20 minutes every hour. For a warm saline rinse, a teaspoon of salt is added to a 12-ounce glass of warm water; the rinse is held in the mouth on the involved side (and spit out) to help relieve the discomfort of trismus. Orally administered aspirin (325 mg) or ibuprofen (600 mg) is usually adequate as an analgesic in managing pain associated with trismus. Their antiinflammatory properties are also beneficial. Diazepam (approximately 10 mg twice daily) or another benzodiazepine is used for muscle relaxation if deemed necessary. The patient should be advised to initiate physiotherapy consisting of opening and closing the mouth, as well as lateral excursions of the mandible, for 5 minutes every 3 to 4 hours. Chewing gum (sugarless, of course!) is yet another means of providing lateral movement of the temporomandibular joint. Record the incident, findings, and treatment in the patient’s dental record. Avoid further dental treatment in the involved region until symptoms resolve and the patient is more comfortable. If continued dental care in the area is urgent, as with a painful infected tooth, it may prove difficult to achieve effective pain control when trismus is present. The VaziraniAkinosi mandibular nerve block usually provides relief of the motor dysfunction, permitting the patient to open his or her mouth, allowing administration of the appropriate injection for clinical pain control, if needed. In virtually all cases of trismus related to intraoral injections that are managed as described, patients report improvement of their condition within 48 to 72 hours. Therapy should be continued until the patient is symptom free. If pain and dysfunction continue unabated beyond 48 hours, consider the possibility of infection. Antibiotics should be added to the treatment regimen described and their use should be continued for 7 days. Complete recovery from injection-related trismus takes about 6 weeks (range, 4 to 20 weeks).76 For severe pain or dysfunction, if no resolution is noted within 2 or 3 days without antibiotics or within 5 to 7 days with antibiotics, or if the ability to open the mouth has become limited, the patient should be referred to an oral and maxillofacial surgeon for evaluation. Other therapies, including the use of ultrasound or appliances, are available for use in these situations.87,88 Temporomandibular joint involvement is rare in the first 4 to 6 weeks after injection. Surgical intervention to correct chronic dysfunction may be indicated in some instances.76,81␣ Soft Tissue Injury Self-inflicted trauma to the lips and tongue is frequently caused by the patient inadvertently biting or chewing these tissues while still anesthetized (see Fig. 17.9). Complications, Legal Considerations, Questions, and the Future 320 PART IV A B • Fig. 17.9 Traumatized lip caused by inadvertent biting while it was still anesthetized. Cause Trauma occurs most frequently in younger children, in mentally or physically disabled children or adults, and in older-old patients (older than 85 years); however, it occurs in patients of all ages. The primary reason is that soft tissue anesthesia lasts significantly longer than does pulpal anesthesia. Dental patients receiving local anesthetic during their treatment are usually dismissed from the dental office with residual soft tissue numbness. (See the discussion in Chapter 20 of phentolamine mesylate, the local anesthesia reversal agent.)␣ Problem Trauma to anesthetized tissues can lead to swelling and significant pain when the anesthetic effects resolve. A young child or a handicapped individual may have difficulty coping with the situation, and this may lead to behavioral problems. The possibility that infection will develop is remote in most instances.␣ • Fig. 17.10 Cotton roll placed between lips and teeth, secured with dental floss, minimizes the risk of accidental mechanical trauma to anesthetized tissues. Prevention A local anesthetic of appropriate duration should be selected if dental appointments are brief. (Refer to the discussion of lip chewing and duration of anesthesia for specific drugs, p. 296.) A cotton roll can be placed in the buccal or labial fold between the lips and the teeth if they are still anesthetized at the time of discharge. The cotton roll is secured with dental floss wrapped around the teeth (to prevent inadvertent aspiration of the roll) (Fig. 17.10). Warn the patient and the guardian against eating, drinking hot fluids, and biting of the lips or tongue to test for anesthesia. A self-adherent warning sticker may be used for children (Fig. 17.11).␣ • Fig. 17.11 Self-adherent warning sticker to help prevent accidental trauma to anesthetized tissues in children. CHAPTER 17 Local Complications 321 Management Management of the patient with self-inflicted soft tissue injury secondary to lip or tongue biting or chewing is symptomatic: 1. analgesics (e.g., age-appropriate dose of ibuprofen) for pain, as necessary; 2. antibiotics, as necessary, in the unlikely situation that infection results; 3. lukewarm saline rinses to aid in decreasing any swelling that may be present; 4. petroleum jelly or other lubricant to cover a lip lesion and minimize irritation.␣ • Fig. 17.12 Hematoma following posterior superior alveolar nerve block. • Fig. 17.13 Hematoma that developed after mental nerve block. Hematoma The effusion of blood into extravascular spaces can be caused by inadvertent nicking of a blood vessel (artery or vein) during administration of a local anesthetic. A hematoma that develops subsequent to nicking of an artery usually increases rapidly in size until management is instituted because of the significantly greater pressure of blood within an artery. Nicking of a vein may or may not result in the formation of a hematoma. Tissue density surrounding the injured vessel is a determining factor. The denser the surrounding tissues (e.g., palate), the less likely a hematoma is to develop, but in looser tissue (e.g., infratemporal fossa), large volumes of blood may amass before a swelling is ever noted and therapy instituted, as is commonly the case when a hematoma develops following a PSA nerve block. Cause Because of the density of tissue in the hard palate and its firm adherence to bone, a hematoma rarely develops after a palatal injection. A rather large hematoma may result from arterial or venous puncture after a PSA nerve block or an IANB. The tissues surrounding these vessels more readily accommodate significant volumes of blood. The blood effuses from vessels until extravascular pressure exceeds intravascular pressure, or until clotting occurs. Hematomas that occur after the IANB are usually visible only intraorally, whereas hematomas that occur after the PSA nerve block are visible extraorally (Fig. 17.12).␣ Problem A hematoma rarely produces significant problems, aside from the resulting “bruise,” which may or may not be visible extraorally. Possible complications of hematoma include trismus and pain. Swelling and discoloration of the region usually subside gradually, with complete resolution occurring between 7 and 21 days. A hematoma constitutes an inconvenience to the patient and an embarrassment to the person administering the drug (Figs. 17.12 and 17.13).␣ Prevention 1. Knowledge of the normal anatomy involved in the proposed injection is important, although keep in mind that “normal” anatomy may differ considerably from patient to patient. Certain techniques are associated with a greater risk of a visible hematoma. The PSA nerve block is the most common, followed by the mental/incisive nerve block and the IANB. 2. Modify the injection technique as dictated by the patient’s anatomy. For example, the depth of penetration for a PSA nerve block may be decreased in a patient with smaller facial characteristics.89,90 3. Use a short needle (27-gauge short needle is recommended) for the PSA nerve block to decrease the risk of hematoma that is commonly a result of needle overinsertion. 4. Minimize the number of needle penetrations into tissue. 5. Never use a needle as a probe in tissues. Hematoma is not always preventable. Whenever a needle is inserted into tissue, the risk of inadvertent puncturing of a blood vessel is present.␣ 322 PART IV Complications, Legal Considerations, Questions, and the Future Management Immediate When swelling becomes evident during or immediately after a local anesthetic injection, direct pressure should be applied to the site of bleeding. No discoloration will be seen at the onset of a hematoma as the blood is relatively deep within the soft tissues. For most injections the blood vessel is located between the surface of the mucous membrane and the bone; localized pressure should be applied for a minimum of 2 minutes. This effectively stops the bleeding. Inferior Alveolar Nerve Block Pressure is applied to the medial aspect of the mandibular ramus. Clinical manifestations of the hematoma, which are visible intraorally, include possible tissue discoloration and probable tissue swelling on the medial (lingual) aspect of the mandibular ramus.␣ Anterior Superior Alveolar (Infraorbital) Nerve Block Pressure is applied to the skin directly over the infraorbital foramen. The immediate clinical manifestation is development of a soft tissue “lump” below the lower eyelid. Discoloration will develop with several hours. Hematoma is unlikely to occur when the technique for anterior superior alveolar nerve block described in Chapter 13 is used, as the application of pressure at the injection site throughout drug administration and for a period of at least 1 to 2 minutes thereafter is recommended.␣ Incisive (Mental) Nerve Block Pressure is placed directly over the mental foramen, externally on the skin or intraorally on the mucous membrane. The initial clinical manifestation is an almost immediate swelling in the mucobuccal fold in the region of the mental foramen, followed in several hours by discoloration of the skin of the chin in the area of the mental foramen (see Fig. 17.13). As with the anterior superior alveolar nerve block, pressure applied during administration of the drug and for a minimum of 1 to 2 minutes following administration effectively minimizes the risk of hematoma formation during incisive (but not mental) nerve block.␣ Buccal Nerve Block or Any Palatal Injection Place pressure at the site of bleeding. In these injections the clinical manifestations of hematoma are usually visible only within the mouth.␣ Posterior Superior Alveolar Nerve Block The PSA nerve block usually produces the largest and most esthetically unappealing hematoma. The infratemporal fossa, into which bleeding occurs, can accommodate a large volume of blood. The hematoma is usually not recognized until a colorless swelling appears on the side of the face around the temporomandibular joint area (usually a few minutes after the injection is completed). It progresses over a period of days, extending inferiorly and anteriorly toward the lower anterior region of the cheek. It is difficult to apply pressure to the site of bleeding in this situation because of the location of the involved blood vessels. It is also relatively difficult to apply pressure directly to the PSA artery (the primary source of bleeding), the facial artery, and the pterygoid plexus of veins. They are located posterior, superior, and medial to the maxillary tuberosity. Bleeding normally ceases when external pressure on the vessels exceeds internal pressure, or when clotting occurs. Digital pressure can be applied to the soft tissues in the mucobuccal fold as far distally as can be tolerated by the patient (without eliciting a gag reflex). Apply pressure in a medial and superior direction. If available, ice should be applied (extraorally) to increase pressure on the site and help to constrict the punctured vessel.␣ Subsequent The patient may be discharged once bleeding stops. Inscribe a note concerning the hematoma in the patient’s dental record. Advise the patient about possible soreness and limitation of movement (trismus). If either of these develops, begin treatment as described for trismus. Discoloration will likely occur as a result of extravascular blood elements; it is gradually resorbed over 7 to 21 days. If soreness develops, advise the patient to take an analgesic such as aspirin or another nonsteroidal antiinflammatory drug. Do not apply heat to the area for at least 4 to 6 hours after the incident. Heat produces vasodilation, which may further increase the size of the hematoma if applied too soon. Heat may be applied to the region beginning the next day. It serves as an analgesic, and its vasodilating properties may increase the rate at which blood elements are resorbed, although the latter benefit is debatable. The patient should apply moist heat to the affected area for 20 minutes every hour. Ice may be applied to the region immediately on recognition of a developing hematoma. Ice acts as both an analgesic and a vasoconstrictor, and it may aid in minimizing the size of the hematoma. Time (tincture of time) is the most important element in managing a hematoma. With or without treatment a hematoma will be present for 7 to 21 days. Avoid additional dental therapy in the region until symptoms and signs resolve.␣ Pain on Injection Pain on injection of a local anesthetic can best be prevented through careful adherence to the basic protocol of atraumatic injection (see Chapter 11). Causes 1. Careless injection technique and a callous attitude (“Palatal injections always hurt” or “This will hurt a little”) all too often become self-fulfilling prophecies. 2. A needle can become dull following multiple insertions. CHAPTER 17 3. Rapid deposition of the local anesthetic solution is more uncomfortable than slow deposition and may cause tissue damage. 4. Needles with barbs (from impaling bone) may produce pain as they are withdrawn from tissue.79␣ Problem Pain on injection increases patient anxiety and may lead to sudden unexpected movement, increasing the risk of needle breakage, traumatic soft tissue injury to the patient, or needlestick injury to the administrator.␣ Prevention 1. Adhere to proper techniques of injection, both anatomic and psychological. 2. Use sharp needles. 3. Use topical anesthetic properly before injection. 4. Use sterile local anesthetic solutions. 5. Inject local anesthetics slowly. The ideal rate is 1.0 mL per minute; the recommended rate is 1.8 mL or a 2.2mL cartridge over 1 minute. 6. Make certain that the temperature of the solution is correct. A solution that is too hot or too cold may be more uncomfortable than one at room temperature. 7. Buffered local anesthetics, at a pH of approximately 7.4, have been demonstrated to be more comfortable on administration.90-92 Buffering of local anesthetics is discussed further in Chapter 20.␣ Local Complications 323 Contamination of local anesthetic cartridges can result when they are stored in alcohol or other sterilizing solutions, leading to diffusion of these solutions into the cartridge. Cartridges stored in cartridge warmers (warmed to normal body temperature) are usually are considered “too hot” by the patient.␣ Problem Although usually transient, the sensation of burning on injection of a local anesthetic indicates that tissue irritation or damage is occurring. If this is caused by the pH of the solution, it rapidly disappears as the anesthetic action develops. Usually no residual sensitivity is noted when the anesthetic action ends. When a burning sensation occurs as a result of rapid injection, a contaminated solution, or an overly warm solution, the likelihood that tissue may be damaged is greater, and subsequent complications, such as postanesthetic trismus, edema, or possible paresthesia, are reported.␣ Prevention No management is necessary. However, steps should be taken to prevent the recurrence of pain associated with the injection of local anesthetics.␣ By buffering the local anesthetic solution to a pH of approximately 7.4 immediately before administration, it is possible to eliminate the burning sensation that some patients experience during injection of a local anesthetic solution containing a vasopressor.90-92 Slowing the speed of injection also helps. The ideal rate of injectable drug administration is 1 mL per minute. Do not exceed the recommended rate of 1.8 mL per minute. The cartridge of anesthetic should be stored at room temperature in the container (blister pack or tin) in which it was shipped, or in a suitable container without alcohol or other sterilizing agents. (See Chapter 7 for proper care and handling of dental cartridges.)␣ Burning on Injection Management Causes Because most instances of burning on injection are transient and do not lead to prolonged tissue involvement, formal treatment is usually not indicated. In those few situations in which postinjection discomfort, edema, or paresthesia becomes evident, management of the specific problem is indicated.␣ Management A burning sensation that occurs during injection of a local anesthetic is not uncommon. Several potential causes are known. The primary cause of a mild burning sensation is the pH of the solution being deposited into the soft tissues. The pH of “plain” local anesthetics (i.e., no vasopressor included) is approximately 6.5, whereas solutions that contain a vasopressor are considerably more acidic (around 3.5 to 4.5). Wahl et al.93 compared the pain on injection of plain prilocaine versus lidocaine with epinephrine (1:100,000) and found no statistical difference in patient perception; however, when bupivacaine with epinephrine (1:200,000) was compared with plain prilocaine, significantly more pain was reported by patients receiving bupivacaine.94 Rapid injection of local anesthetic, especially in the denser, more adherent tissues of the palate, produces a burning sensation. Infection Infection subsequent to local anesthetic administration in dentistry is an extremely rare occurrence since the introduction of single-use sterile needles and glass cartridges. Causes The major cause of postinjection infection is contamination of the needle before administration of the anesthetic. Contamination of a needle always occurs when the needle 324 PART IV Complications, Legal Considerations, Questions, and the Future touches mucous membrane in the oral cavity. This cannot be prevented, nor is it a significant problem because the normal bacterial flora of the oral cavity does not lead to tissue infection. Improper technique in the handling of local anesthetic equipment and improper tissue preparation for injection are other possible causes of infection. Injecting Local Anesthetic Solution Into an Area of Infection As discussed in the section on local anesthetic requirements in endodontics in Chapter 16, local anesthetics are considerably less effective when injected into infected tissues. However, if they are deposited under pressure, as in the periodontal ligament injection, the force of their administration might transport bacteria into adjacent, healthy tissues, thereby spreading infection.␣ Problem Contamination of needles or solutions may cause a lowgrade infection when the needle or solution is placed in deeper tissue. This may lead to trismus if it is not recognized and proper treatment is not initiated.61␣ Prevention 1. Use sterile disposable needles. 2. Proper care and handling of needles. Take precautions to avoid contamination of the needle through contact with nonsterile surfaces; avoid multiple injections with the same needle, if possible. 3. Proper care and handling of local anesthetic cartridges. a. Use a cartridge only once (one patient). b. Store cartridges aseptically in their original container, covered at all times. c. Cleanse the diaphragm with a sterile disposable alcohol wipe immediately before use if considered necessary. 4. Properly prepare the tissues before penetration. Dry them and apply topical antiseptic (optional).␣ Management Low-grade infection, which is rare, is seldom recognized immediately. The patient usually reports postinjection pain and dysfunction (e.g., trismus) 1 day or more after their dental treatment. Overt signs and symptoms of infection occur rarely. Immediate treatment consists of those procedures used to manage trismus: heat and analgesic if needed, muscle relaxant if needed, and physiotherapy. Trismus produced by factors other than infection normally responds with resolution or reduction within several days. If signs and symptoms of trismus do not begin to respond to conservative therapy within 3 days, the possibility of a lowgrade infection should be entertained and a 7- to 10-day course of antibiotic therapy should be started. Prescribe 29 (or 41, if 10 days) tablets of penicillin V (250-mg tablets). The patient takes 500 mg immediately and then 250 mg four times a day until all tablets have been taken. Erythromycin may be substituted if the patient is allergic to penicillin. Record the progress and management of the patient in the dental record.␣ Edema Swelling of tissues is not a syndrome but it is a clinical sign of the presence of some disorder. Causes 1. Trauma during injection. 2. Infection. 3. Allergy: angioedema is a possible response to ester-type topical anesthetics in an allergic patient (localized tissue swelling occurs as a result of vasodilation secondary to histamine release). 4. Hemorrhage (effusion of blood into soft tissues produces swelling). 5. Injection of irritating solutions (alcohol-containing cartridges or cold sterilizing solution–containing cartridges). 6. Hereditary angioedema is a condition characterized by the sudden onset of brawny nonpitting edema affecting the face, extremities, and mucosal surfaces of the intestine and respiratory tract, often without obvious precipitating factors. Tissue manipulation within the oral cavity, including local anesthetic administration, may precipitate an attack. Lips, eyelids, and the tongue are often involved.95 Karlis et al.96 noted that 15% to 33% of untreated angioedema patients died of acute airway obstruction as a result of laryngeal edema.␣ Problem Edema related to local anesthetic administration is seldom of sufficient intensity to produce significant problems such as airway obstruction. Most instances of local anesthetic– related edema result in pain and dysfunction of the region and embarrassment for the patient. Angioneurotic edema produced by a topical anesthetic in an allergic individual, although exceedingly rare, can compromise the airway. Edema of the tongue, pharynx, or larynx may develop, and is a potentially life-threatening situation that requires vigorous management (including activation of emergency medical services).97␣ Prevention 1. Proper care and handling of the local anesthetic armamentarium. 2. Use atraumatic injection technique. 3. Complete an adequate medical evaluation of the patient before drug administration.␣ CHAPTER 17 Management The management of edema is predicated on reduction of the swelling as quickly as possible and on the cause of the edema. When produced by traumatic injection or by introduction of irritating solutions, edema is usually of minimal degree and resolves in several days without formal therapy. In this and all situations in which edema is present, it may be necessary to prescribe analgesics for management of pain. After hemorrhage, edema resolves more slowly (over 7 to 21 days) as extravasated blood elements are resorbed into the vascular system. If signs of hemorrhage (e.g., bluish discoloration progressing to green, yellow, and other colors) are evident, management follows that previously discussed for hematoma. Edema produced by infection does not resolve spontaneously but may become progressively more intense if untreated. If signs and symptoms of infection (pain, mandibular dysfunction, edema, warmth) do not appear to resolve within 3 days, antibiotic therapy should be instituted as outlined previously. Allergy-induced edema is potentially life threatening. Its degree and location are highly significant. If swelling develops in buccal soft tissues and there is absolutely no airway involvement, treatment consists of immediate intramuscular injection (in the vastus lateralis muscle) of 50 mg (adult) or 25 mg (child up to 30 kg) followed by a 3-day course of oral histamine blocker therapy and consultation with an allergist to determine the precise cause of the edema. If edema occurs in any area where it compromises breathing, treatment consists of the following: 1. P (position): if unconscious, the patient is placed supine. 2. C-A-B (circulation, airway, breathing): basic life support is administered, as needed. 3. D (definitive treatment): emergency medical services (e.g., 9-1-1) are summoned. 4. Epinephrine is administered: 0.3 mg (0.3 mL of a 1:1000 epinephrine solution) for weight greater than 30 kg), 0.15 mg (0.15 mL of a 1:1000 epinephrine solution) for weight between 15 and 30 kg, IM in the vastus lateralis every 5 minutes until respiratory distress resolves. 5. Histamine blocker is administered intramuscularly or intravenously. 6. Corticosteroid is administered intramuscularly or intravenously. 7. Preparation is made for cricothyrotomy if total airway obstruction appears to be developing. This is extremely rare but is the reason for summoning emergency medical services as quickly as possible. 8. The patient’s condition is thoroughly evaluated before his or her next appointment to determine the cause of the reaction.␣ Local Complications 325 Causes Epithelial Desquamation 1. Application of a t