Anesthetic Techniques Involved

• Mandibular block with the conventional or direct technique (Kronman and Giunta 1987; Heasman and Reid 1995; Webber et al. 2001; Uckan et al. 2006; Paul et al. 2009; Aravena et al. 2016), the Gow‐Gates technique (Dryden 1993) or the Laguardia–Akinosi technique (Donkor et al. 1990).
• In the maxillary arch, the techniques involved are buccal infiltration, posterior superior alveolar nerve block, the high tuberosity technique (Kronman and Giunta 1987; Lustig and Zusman 1999), and the transpalatal (greater palatine canal) approach (Mercuri 1979).

Clinical Manifestations

Blanching appears on the same side of the face as the injection, with the following:

1. Facial blanching, which is characterized by the following:
   • Onset on the skin of the face below the lower eyelid (infraorbital), malar or zygomatic region, side of the nose, and above the nasolabial fold (cheek). It manifests as a continuous white patch (Figure 22.1) or occasionally two patches (Kronman and Giunta 1987). Blanching is easily observed in persons whose skin is not black (Mercuri 1979) and disappears spontaneously after 10–30 minutes (Kronman and Giunta 1987; Heasman and Reid 1995; Paul et al. 2009; Aravena et al. 2016; Kumaresan et al. 2018).
   • The patch can sometimes extend intraorally to the maxillary gingiva (Heasman and Reid 1995; Aravena et al. 2016), hard palate (Dryden 1993; Heasman and Reid 1995; Aravena et al. 2016; Kumaresan et al. 2018), or even to the lower lip (Webber et al. 2001).
   • An asymptomatic sign (only observed by the dentist), although the patient may initially feel numbness, itching, a burning sensation, or even shooting pain, in the affected area (Mercuri 1979; Webber et al. 2001; Uckan et al. 2006; Paul et al. 2009; Aravena et al. 2016; Kumaresan et al. 2018).
2. While rare, ocular complications (see section “Ocular Complications”) of the have been described (Dryden 1993; Webber et al. 2001; Chiappelli and Cajulis 2002; Uckan et al. 2006) and include the following:
   

   

   • Double vision (diplopia).
   • Sensation of numbness, burning, or even pain in the eye and periorbital area.
   • Drooping of the upper eyelid (ptosis).
   • Ischemic paling may extend to the eyelids and forehead (Webber et al. 2001; Uckan et al. 2006).

   In these cases, ocular manifestations are the main event, with blanching no more than an accompanying sign.

Causes and Pathophysiology

Clinical Manifestations

The affected skin depends on the region where the anesthesia is injected. Thus, in cases of mandibular block, the skin of the lower lip is affected above the chin or adjacent to the commissure; the skin of the upper lip is affected in maxillary infiltrations.

Clinical manifestations appear during the first hours (30 minutes to 3 hours) after administration of the anesthetic (rarely before 3 days) (Table 22.4) and are characterized by the appearance of a reddish patch (erythematous macule), which is usually accompanied by itching (pruritus) or a burning sensation. Occasionally, it first manifests as a pale patch that progresses to an erythematous macule within a few hours (Torrente‐Castells et al. 2008).

During the following days or weeks, the lesion progresses to necrosis of the skin with formation of a crust that leaves a pigmented or hypopigmented area or simply a scar on healing. Sensory alterations on the chin are a potential sequela (Krüger and Nehse 1991).

Causes and Pathophysiology

The causes are not well known, although two possible mechanisms have been posited (Curley and Baxter 1987):

Technical Factors Contributing to Hematomas

The techniques that most frequently lead to hematomas on the face are as follows:

1. Injections into the area of the upper molars in buccal infiltration, posterior superior alveolar nerve block, and high tuberosity approaches (Bennett 1984; Laskin 1984; Roberts and Sowray 1987; Jastak et al. 1995; Malamed 2004). At this level, 0.5% of injections can lead to facial hematoma (Kuster and Udin 1984), especially when the needle is inserted higher and deeper, since it is easier to inject into a branch of the pterygoid venous plexus or the posterior superior alveolar artery (Harn et al. 2002).
2. Block applied at the level of the foramina (infraorbital and mental) (Laskin 1984; Roberts and Sowray 1987; Joyce and Donnelly 1993; Jastak et al. 1995; Malamed 2004; Karkut et al. 2010). With some exceptions and specific cases such as those already discussed, these techniques are not recommended in current practice (Evers and Haegerstam 1981; Kleier et al. 1983; Haglund and Evers 1985; Joyce and Donnelly 1993).

Clinical Manifestations

• Swelling, which appears in the area of the upper molars (Kuster and Udin 1984) and can appear on the skin of the malar region or masseter. This swelling is very large and cosmetically undesirable because a large quantity of blood can accumulate in the infratemporal space, thus highlighting the resulting facial asymmetry (Malamed 2004). Swelling appears rapidly if the lesion affects an artery, such as a branch of the facial artery or a buccogingival branch of the posterior superior alveolar artery, which follows an irregular path along the maxillary tuberosity (Jastak et al. 1995; Harn et al. 2002; Malamed 2004), or slowly if the lesion affects a vein of the pterygoid venous plexus (Jastak et al. 1995; Malamed 2004).
• Skin discoloration, also known as ecchymosis (Bennett 1984; Kuster and Udin 1984; Roberts and Sowray 1987; Malamed 2004), progresses downwards and forwards along the muscle planes of the cheek until it reabsorbs spontaneously after 10–15 days (Malamed 2004).
• Other occasional manifestations include the following:
  • Sensation of tightness, but not pain, in the area affected (Jastak et al. 1995).
  • Difficulty opening the mouth (trismus) if the tip of the needle has irritated the lateral (external) pterygoid muscle (Malamed 2004).

Management by the Dentist

• The patient should be advised that the hematoma reabsorbs within 10–15 days (Bennett 1984; Malamed 2004). Often no interventions are recommended and invasive measures such as drainage are contraindicated (Bennett 1984; Roberts and Sowray 1987; Jastak et al. 1995; Malamed 2004).
• If the swelling is detected early, the dentist may attempt to control it by pressing on the affected area for 15 minutes (Kuster and Udin 1984; Laskin 1984) and/or applying ice to the skin for its vasoconstrictive effect (Kuster and Udin 1984; Jastak et al. 1995; Malamed 2004). In the case of a hematoma affecting the region of the upper molars, it is difficult to apply direct pressure, therefore a finger should be inserted directly into the mouth and pressure applied at the bottom of the vestibular surface of the upper molars, whereas on the outside pressure can be applied to the skin of the malar region (Malamed 2004).
• As an option, some authors recommend that the patient apply heat to the affected area 24 hours after the procedure to aid reabsorption of the hematoma (Laskin 1984; Jastak et al. 1995; Malamed 2004). Heat causes vasodilation, favors withdrawal of the extravasated blood, and has an analgesic effect.
• Some authors suggest reassessing the lesion at 48 hours to determine whether an infection has developed (very unusual) and prescribe antibiotics (Laskin 1984).

Anatomical Lesions

In 1943, Seddon described three basic types of lesion of the peripheral nerves (Seddon 1943):

• Neurapraxia. When there is no axonal degeneration, although the axons are intact, they do not conduct electrochemical impulses. There is no loss of axonal continuity. In these cases, recovery is spontaneous (10 days to 3 weeks).
• Axonotmesis. When there is axonal degeneration. There is no anatomical damage to the nerve, and although the axon is split, the nerve stem remains intact thanks to the supporting connective tissue. Recovery is spontaneous (6–8 weeks or 2–6 months).
• Neurotmesis. When there is axonal degeneration and anatomical damage to the nerve and therefore complete rupture of the nerve stem. The resulting lesion is permanent and a scar neuroma may form as a result of interference in neuronal regeneration.

General Causes

1. Needle injury (physical effect). The tip of the needle, especially if barbed outwards (typical in mandibular block after pressing the needle against the bone) (Stacy et al. 1994), can directly injure the nerve stem and lead to intraneural hemorrhage (Haas and Lennon 1995; Pogrel and Thamby 2000) (Figure 22.2), which in turn could increase pressure on the nerve fibers, thus altering metabolism and nerve function (Haas and Lennon 1995). The situation is aggravated by the subsequent intra‐ and extraneural fibrosis (Pogrel and Thamby 2000).

   Repeating the number of injections, especially in mandibular block, increases the risk of this type of lesion (Pogrel et al. 1995; Pogrel and Thamby 2000; Hillerup and Jensen 2006). In some series, 35% of patients report having received more than two injections at the same site (Hillerup and Jensen 2006).

   

   Note: It is interesting that, in five cases involving exploratory surgery, no evidence of needle‐induced microtrauma was observed, although the area was slightly pale and there were adhesions around the nerve (Pogrel and Thamby 2000).

2. Neurotoxicity caused by contamination of anesthetic solution (chemical effect). For some time, professionals had a bad habit of submerging the local anesthesia cartridges in surface disinfectants, often alcohol, with the result that the disinfectant entered the cartridge through the diaphragm or the rubber plunger (made from semipermeable membranes), thus making the injection more painful and irritating the tissues and, more importantly, the nerve (Shannon and Feller 1972; Shannon and Wescott 1974).
3. Neurotoxicity caused by the individual components of the local anesthesia solution (chemical effect). Experiments with animals (Lundy et al. 1933; Tui et al. 1944; Skou 1954; Fink and Kish 1976; Myers et al. 1986; Kalichman et al. 1993) have demonstrated the neurotoxic effect of local anesthetics, especially when these are used at high concentrations. Clinical studies have also demonstrated this adverse effect in medical practice (Rigler et al. 1991) and in dental practice (Nickel 1990; Haas and Lennon 1995; Miller and Haas 2000; Van Eeden and Patel 2002; Hillerup and Jensen 2006; Garisto et al. 2010), especially when high concentrations are administered, as is the case with lidocaine 5% (Rigler et al. 1991), articaine 4% (Haas and Lennon 1995; Miller and Haas 2000; Van Eeden and Patel 2002; Hillerup and Jensen 2006; Hillerup et al. 2011; Garisto et al. 2010), and prilocaine 4% (Haas and Lennon 1995; Miller and Haas 2000; Garisto et al. 2010).

Immediate Electric Shock Sensation

Immediate electric shock sensation (cramp) is mainly felt in mandibular block. When the needle is inserted, the patient experiences a sudden and short electric shock sensation, which is like an intense burning sensation along the nerve that has been touched by the tip of the needle (lingual nerve or inferior alveolar nerve). The sensation lasts a second but is very unpleasant for the patient, although it has the advantage of producing deep and quick anesthesia with a small amount of anesthetic solution.

The frequency of electric shock sensation in mandibular block is around 3% (Table 22.5), and this is more common in the lingual nerve than in the inferior alveolar nerve (ratio 4:1). In the case of the lingual nerve, the area affected by the sensation is the tongue on the side the anesthetic is injected; in the case of the inferior alveolar nerve, the area affected is the half of the lower lip on the side which the anesthetic is injected.

When faced with these situations in the office, we advise the following:

• Show the patient that you are aware how unpleasant the sensation is and state that this happens because the anesthetic was injected immediately above the nerve, when the normal approach is to inject it to the side.
• Tell the patient that the discomfort has the advantage that the anesthetic effect is quicker and stronger.
• In cases where this accident is repeated in the same patient, we advise against using mandibular block because it indicates a possible anatomical abnormality and repeated injury could carry a risk of long‐term paresthesia. As alternatives, we propose the use of another mandibular block technique such as Gow‐Gates (Chapter 16) or infiltrative techniques accompanied by intraligamentary or intraosseous approaches (Chapter 18).

Long‐Term Paresthesia

The frequency of long‐term paresthesia or nonsurgical neuropathy caused by dental local anesthesia is unknown (Pogrel and Thamby 2000; Hillerup and Jensen 2006); however, some authors provide estimates, although these vary widely, ranging from 1:5000 injections to 1:14 million injections (Table 22.6). Clinical experience tells us that cases of long‐term paresthesia are not often seen in clinical practice, therefore a frequency ranging from 1:5000 to 1:10 000 seems excessive. Furthermore, the study by Garisto et al. (2010), which reported a frequency of 1:14 million, recognizes that this is improbable and that the frequency may be even greater. We believe that the true value lies somewhere between the figures reported (Table 22.6), that is, a median of 1 : 100 000 injections.

By far the most frequently involved technique is mandibular block (99%) (Table 22.7) and the most frequently involved nerves are the lingual nerve (70%, tongue involvement), the inferior alveolar nerve (20%, involvement of half of the lower lip), and both nerves (10%) (Table 22.7). The reason for more frequent involvement of the lingual nerve seems to be that in 33% of cases it is composed of a single bunch of nerve fibers (possibly one to eight), whereas the inferior alveolar nerve is composed of three to 14 bundles, therefore injury is offset by the remaining healthy bundles (Pogrel et al. 2003; Khoury et al. 2010). Also, the inferior alveolar nerve may be partially protected from oncoming the needles by a crest of thickened bone, which bulges anteriorly in the sulcus colli, and the protection of the lingula (Khoury Mihailidis et al. 2011). In contrast, the lingual nerve is quite bare, with no bony protection, exposing it to an increased risk of direct contact during needle insertion due to its anteromedial position (Khoury Mihailidis et al. 2011) (Figure 3.14, Chapter 3).

Alterations of the Sense of Taste

Ten percent of the fibers of the facial nerve (CN VII) leave the nerve 15 mm after exiting the stylomastoid foramen. After a varied course, they join the upper border of the lingual nerve to form the chorda tympani, which also carries special visceral afferent (taste) fibers from the anterior two‐thirds of the tongue as well as general visceral efferent parasympathetic fibers that synapse at the submandibular ganglion and go on to provide innervation of the sublingual and submandibular glands.

Injury to these fibers leads to reduced sense of taste (hypogeusia) on the affected side of the tongue or even total disappearance of the sense of taste (ageusia) for sugar‐sweet, salty, bitter, and acid‐lemon flavors, as assessed using gustometry (Paxton et al. 1994; Hillerup and Jensen 2006). Atrophy of the fungiform papillae on the affected side of the tongue may also be observed (Cowan 1990).

Of note, there have been three cases of involvement of the sense of taste only, with no other nervous abnormality. None of the three recovered within a year (Paxton et al. 1994; Pogrel and Thamby 2000).

Hoarseness

There have been few reports of hoarseness immediately after injection in mandibular block. Hoarseness was accompanied by dysphagia and breathing difficulty, which lasted 2–3 hours before resolving without sequelae. The cause is thought to be recurrent laryngeal nerve block (branch of the vagus nerve, CN X) because of an anatomical variation (Cilasun et al. 2012).

Local Anesthetic Techniques Implicated in the Development of Trismus

1. Mandibular block, which irritates the medial (internal) pterygoid muscle (Stone and Kaban 1979; Stacy et al. 1994). The technique leads to trismus in 3% of cases (Table 22.11) and accounts for 95% of all cases of trismus (Table 22.12).
2. In the upper arch, posterior superior alveolar nerve block or the high tuberosity approach. When applied in the area of the maxillary molars, these techniques can irritate the lateral (external) pterygoid muscle (Stone and Kaban 1979; Shaner et al. 2007) and account for 5% of all cases (Table 22.12) as compared to trismus following mandibular block.

Causes of Trismus

1. Mechanical injury or irritation of the pterygoid muscles (medial and lateral) by the tip of the needle
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