This is the fifth of seven pages which constitute a course in local anesthetics. Each page stands on its own, however for a thorough understanding of dental local anesthetics the reader is advised to read the pages in order.
Joint Hypermobility Syndrome (JHS) also called HyperMobility Syndrome (HMS), is one of a group of inherited conditions which affect the connective tissues of the body. It is estimated that 10%-15% of normal children have hypermobile joints, or joints that can move beyond the normal range of motion. Patients with these conditions are more prone to joint injuries than patients without. The problems associated with JHS seem to diminish with age, and persons born with less severe forms of HMS may be unaware of their condition. The most severe variant of HMS is called Ehlers-Danlos syndrome. Persons with this rare variant generally are well aware that they have a some sort of joint and muscle problem, even if they are not exactly sure of what is causing it.
Studies have suggested that as many as half of JHS patients have enhanced pain perception as well as noticeable pain in multiple sites in the body. Many seem to respond poorly to local anesthetics (i.e., at the dentist or during surgery) and require larger dosages for effective pain control. Most of the evidence for the lack of efficacy of local anesthetics in patients suffering from less severe form of HMS is anecdotal, so it is difficult to say with certainty that a patient who seems refractory to local anesthetics is in fact suffering from a side effect of an undiagnosed case of JHS. If a refractory patient has had a lot of accidental joint injuries, or knows he or she is "double jointed", this would be a reasonable avenue to explore.
In patients suffering from the various forms of HMS, the local anesthetic will produce numbness, but it may be of insufficient intensity or duration to complete the dental procedure without repeated injections. The reason probably involves the rapid absorption of the anesthetic solution into the bloodstream due to the defective nature of the connective tissues in the surrounding blood vessels. If the anesthetic solution cannot remain in place long enough to take effect, then the patient will not get numb. The best way to combat this problem is to use a long acting anesthetic like bupivicaine (Marcaine) with vasoconstrictor.
There is a general consensus in dentistry that patients directly under the influence of large amounts of alcohol, as well as recovering alcoholics can be quite difficult to get numb in the dental office. A few studies have confirmed this supposition with respect to alcoholics in hospital settings, although most of the evidence suggesting that alcohol directly affects the efficacy of local anesthetics appears to be anecdotal.
The mechanism for the direct effect of alcohol on the ability of anesthetic solution to produce numbness would be a combination of systemic acidosis and reduced circulatory resistance due to the vasodilative properties of alcohol.
High alcohol intake produces a state of metabolic acidosis which affects all the tissues of the body. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis. An acidic environment at the site of the injection reduces the ability of the anesthetic to cross the cell membrane into the nerves, thus limiting its effects. A good discussion of this is found on page 4 of this course, and I advise persons who want to know more about the physiology of nerves and local anesthesia to read the entire page, but the specific reference to acid/base balance is found here.
Alcohol acts as a vasodilator. In other words, it causes relaxation of the smooth muscles that line the blood vessels, at least during the initial stages of inebriation. This causes them to widen (dilate) and increases the volume of blood that flows through them. One obvious sign that this is happening is the tendency of persons who are drunk to have flushed faces. Vasodilation also occurs at deeper levels, and the increased blood flow at the site of the injection carries away the anesthetic bolus more quickly than would otherwise be the case. This reduces the time during which the anesthetic solution is available to produce its effect.
No one is immune to the effect of local anesthetic!
If the patient suffers from one of the various forms of HMS, they may require much more anesthetic with repeated injections, but they can usually be made sufficiently numb to proceed with dental work if enough anesthetic is injected. When a patient does not get numb for a procedure in spite of a dentist's best efforts, the reason is generally that the anesthetic has either not reached the nerve, or has not penetrated into the nerve. Remember that a dentist never intentionally gives a shot directly into a nerve trunk. He/she simply delivers the anesthetic solution into close approximation with the relevant nerve fibers and hopes that the material diffuses through the intervening structures, surrounds the nerve fibers and then diffuses into them. In order to understand how failures in anesthesia happen, it is helpful to understand a bit about the techniques of delivery of the shots.
A field block is often called an "infiltration". It is a shot that is delivered into the gums directly beside the tooth or teeth that the dentist wants to anesthetize. Since the introduction of articaine (Septocaine), which is quite good at diffusing through bone, field blocks have become useful on 26 of the 32 teeth (lower molars are the exception). The needle is inserted a very short distance into the movable buccal or labial tissue at about the level of the tip of the root, and the anesthesia is delivered there. The solution then diffuses through the periosteum (the thin covering of the bone) and then through the thin layer of bone that surrounds the tip of the root where the nerve enters the tooth. Using articaine which diffuses through bone very well, this procedure is effective on all premolars and anterior teeth regardless of location in upper or lower arch. The advantage of a field block is that there is never a question in the dentist's mind about the location of the spot where the anesthesia should be delivered, or about the depth of the shot. The needle enters the tissue at about where the dentist estimates the tip of the root lies, and penetrates no more than 1/8 inch. Hence there in never a likelihood of "missing" the block.
There are only two things that may interfere with the production of numbness during a field block:
Very thick or dense bone
Even articaine cannot diffuse through very dense or very thick bone. This is most likely to be a factor in lower molars and lower canine teeth. If dense or thick bone is the factor preventing the induction of anesthesia, then the dentist must resort to a major nerve block to anesthetize these teeth.
Infected tissue tends to be acidic. Acidic tissue does not anesthetize easily. See my discussion of PKa for a better understanding of this phenomenon. This is a function of chemistry. It is generally best to treat an infection prior to giving a shot in the area to be anesthetized mostly because injections into infected tissue are not only painful, but often ineffective.
Major nerve blocks are necessary to anesthetize all molars, and there is a major nerve block available for each of the other teeth as well, even the ones generally anesthetized with field blocks. When giving a major nerve block, the dentist aims for a deeply placed bundle of nerves, or a nerve trunk which contains fibers from the area he wants to anesthetize. The nerve trunk also contains fibers from adjacent areas, so the area of numbness may encompass the entire lower jaw, or even the entire side of the head depending on the target of the block.
There are essentially two reasons why a major nerve block might not produce the anesthetic effect one would expect. The first is what I call the hot tooth syndrome. The second involves variations in individual internal anatomy.
The hot tooth syndrome
Every dentist encounters the occasional "hot tooth" which refuses to get numb, even when using a major block. While it is easy to explain the failure of a field block delivered into the local inflamed tissue, namely acidic PH blocking entry of the anesthetic into the nerve, it is more difficult to invoke the same explanation when speaking of a major nerve block administered in a facial plane distal and separated from the one in which the infection has resulted in localized pH changes.
The mystery of the tooth that refuses to get numb
To be honest, I do not know of a scientifically valid reason for the hot tooth syndrome, but I will advance a theory in the hopes that someone out there might have a better explanation.
I believe that a localized acidosis, even one isolated inside a pulp chamber, might affect the entire nerve bundle, including all of the connective tissue, blood vessels and neuronal elements. Baring that, even if it does not affect the connective tissues and blood vessels, it would, at minimum, affect all of the the nerve fibers that originate in the affected tooth itself. This would include the neuron cell bodies, the dendrites and the entire length of the axons that extend from them .
In a sense, the acidosis “travels” up toward the semilunar ganglion. Every dentist knows that pain in a hot tooth leads to hypersensitivity, as well as referred pain over the entire distribution of the bundle, and even to other branches of the trigeminal nerve. If "traveling acidosis" affects the nerve bundle, or the affected nerve fibers inside the bundle at the site of the injection, then the absorption of the anesthetic would be inhibited there, as well as locally around the tooth itself.
Variations in individual internal anatomy
Major nerve blocks require the use of longer needles and are somewhat more dependent on local anatomic variations in the patient's anatomy. Everyone has two eyes, a nose and a mouth, but variations in the anatomy of these gives everyone a unique appearance. We are like that internally too. Since a vast majority of people have anatomy that fits within certain norms, dentists use techniques that generally guide the tip of the needle to the target using external anatomy as a guide to the hidden anatomy underneath. Unfortunately, some patients have hidden internal anatomy that does not fit within the standard variation, and therefore, a dentist may "miss" the block simply because of this anatomic variation.
Furthermore, the longer needle is more likely to deviate from a straight path direct to the target structure causing a missed block. This happens because of the flexibility of the needle combined with the "aerodynamic" characteristics of the bevel of the needle which acts like a rudder causing the tip of the needle to deviate from the straight path.
The Gow-Gates Block
The most commonly delivered major nerve block is the mandibular nerve block. It is the shot that normally makes one half of the entire lower jaw numb, along with half the tongue. It is one of the most important major nerve blocks in dentistry, and, unfortunately, also one of the most commonly "missed blocks". Failure to obtain good anesthesia with a mandibular block is very frustrating to both the dentist and the patient. The most common reason for failure of this block is variation in patient anatomy.
A great alternative to the standard mandibular block was invented by an Australian dentist named Gow-Gates. When properly delivered, it is painless, and nearly 100% effective with a very fast onset of anesthesia. The dentist aims the tip of the needle for the neck of the condyle, aspirates and delivers the entire carpule. No lingual, long buccal, or any other accessory injection is necessary since the mandibular nerve is anesthetized before any of these branches split off.
The only problem with this block has been that until now, there has been no reliable method for "finding" the target. Over a period of years, I have developed a very simple technique which reliably finds the target and has vastly simplified the practice of dentistry for me. I have written a page for other dentists that demonstrates my technique. If you try it and can improve on it, let me know.
To my knowledge, there isn't much research on this subject, so what follows is based on my own observations. Any dentist, physician or academic is welcome to e-mail me with their views.
I believe that severe anxiety on the part of a patient can affect the effectiveness and duration of local anesthetic, although, even extremely anxious patients can be made numb if enough anesthesia is injected. The following are the factors that I believe may be involved in causing this phenomenon:
Anxious patients are likely to have abnormal body PH. It may involve alkalosis if the patient is hyperventilating, or acidosis due to hyperactivity of the skeletal musculature. Any deviation of local PH from normal can affect the ability of the anesthetic radicals to penetrate the nerve cell (axon) membrane. Please see my explanation of PKa above for a better understanding of this phenomenon. This would affect both field blocks and major nerve blocks.
People who are anxious in the dental chair are likely to be bruxers (people who unconsciously grind or clench their teeth). People who brux are likely to have extremely sensitive teeth, and again, though research in this area is scant, I believe the reason for the extreme sensitivity is due to inflammation of the hammock ligament at the tip of the root caused by the constant stress placed on it by the bruxing habit. Inflamed tissue remains in a state of acidosis which would prevent diffusion of the anesthetic into the nerve bundle at that point. This would limit the effectiveness of field blocks (infiltrations).
Under any circumstance, severely anxious patients may be better served, and better anesthetized, if prescribed diazepam (Valium) tablets, 10 - 15 mg to be taken an hour before presenting to the office. Patients so sedated should never drive under the influence and should be accompanied by an adult driver in transit to and from the office.
Most injections are not especially painful. We are not actually trying to "hit" a nerve when we penetrate, and since the majority of the pain sensors are located in the surface mucosa, the use of a topical anesthetic can be quite helpful in preventing most sensation. The techniques are designed to allow needle penetration with the least trauma to known existing structures under the mucosa. Unfortunately, variations in internal anatomy can occasionally place a sensitive structure in the path of the needle. When we give a lower nerve block, the needle penetrates beside the lingual nerve. If variations in anatomy place the lingual nerve directly in the path of the needle, the patient will often feel a burning jolt in the tongue. It is very quick, but quite surprising and sometimes scary. It generally does not cause serious injury. However, the patient may experience prolonged numbness or paresthesia (burning or tingling sensation) in the tongue for up to three weeks (sometimes a number of months) after the procedure. This same phenomenon may happen to other nerves causing a jolt to radiate into the lower jaw, down the neck or behind the ear. Once again, no damage done. Just an unwanted complication.
It has been my experience that the probability of hitting a nerve increases if the patient is especially thin. When one gains or looses weight, the neurovascular bundles (blood vessels and nerves run together in bundles) do not increase or decrease in diameter. It is a modern social convention today that "you can't be too thin", however thin people lack bulk in the muscle and fat surrounding the spaces where the injection is aimed. This makes the relative size of the neurovascular bundle larger with respect to the rest of the target. The nerve becomes a "larger needle in a smaller haystack", and thus more likely to be struck directly by the needle.
If the tip of the needle enters an artery, the patient may experience pain and blanching on the skin of the neck and face. This is due to the fact that most injections use vasoconstrictor. The anesthesia is swept along the distribution of the artery into the arterioles and capillaries of the skin and muscle and the vasoconstrictor causes these blood vessels to temporarily close down causing ischemia (lack of blood flow) in the tissue. Ischemia is a painful, but temporary condition. If this happens, the dentist generally stops the injection. No permanent damage is done, but the patient may lose some confidence in the dentist. In order to avoid this complication, the dentist generally develops an injection technique in which he "aspirates" (pulls back on the plunger of the syringe) in order to see if any blood enters the carpule. If this happens (very rarely) he changes the position of the needle and aspirates again.
Injection into a neurovascular bundle
Make no mistake. Local anesthesia is serious medicine, and a dental injection is a serious surgical procedure. Some people are more susceptible to negative local toxic effects of the anesthetic agent or the associated vasoconstrictor than most, and these people may suffer some local negative and (generally) temporary side effects from the agents. Injection directly into a nerve trunk may unintentionally happen after the patient is already numb and unable to feel the intrusion. Injection directly into a neurovascular bundle (nerve trunk) may cause physical damage due to the expansion of the anesthetic bolus, local toxic effects of the agent and ischemia in the nerve from the vasoconstrictor. The vast majority of these complications slowly heal and are gone over a period of several weeks or months. Upon rare occasion, they can last quite a bit longer (over a year), but if the patient waits it out, the injury will generally heal.
Physical reaction to the anesthetic itself
Local anesthetic agents that come in higher concentrations such as articaine and prilocaine have been implicated in a very slightly higher incidence of this complication. This most commonly occurs in major nerve blocks of the lower jaw. At this time, no one knows why this happens, but it is a fairly rare complication.
Sometimes the tip of the needle may penetrate under the periosteum which is the thin, tough covering of the bone. When this happens, the periosteum is separated from the surface of the bone and serious pain can result when the anesthesia wears off. In spite of the severity of the pain, the damage is temporary and generally is gone within 12 hours.
It is not uncommon for patients to feel nervous with a fast heart rate immediately after receiving a shot of local anesthetic. This generally happens when an anesthetic with a vasoconstrictor is being used. In these cases, the vasoconstrictor is entering into larger veins and going into general circulation. The vasoconstrictor is the same as the naturally occurring "fight or flight" hormone adrenaline, and it is acting just like the release of natural adrenaline would to produce a heightened sense of awareness, nervousness and an increased heart rate. This is a short lived reaction and is generally not dangerous. The feeling fades after a minute or two and the patient feels much better.