Analgesia and Infection

[troy2k]

First, I will admit that I had terrible luck trying to find ANYTHING on this subject. However, here's what I've pieced together on the physiology of the subject.
There are 3 major features underlying inflammatory pain: a change in the peripheral sensitivity of high-threshold nociceptors--ie, increased sensitivity; an alteration in the chemical makeup of the neurons in the nervous system, a change in their properties and function-- called a phenotypic switch; and finally an increase in the excitability or the responsiveness of neurons within the central nervous system, and this represents central sensitization.
More importantly maybe is the proliferation of proteolytic substances, which may be responsible for the destruction (lysing) of opioid and amide receptor sites, inhibiting analgesic response.
As I said, at this point in time I found NO specific references to the phenomenon of decreased analgesia due to local infection. I have however researched this before. At that time there was little if any understanding as to the mechanisms involved. Much of this is still theory on my part, and I'd be glad to hear what others have found.
Now the important stuff: if you have a patient who falls into this category, it becomes a question of priorities. Will his peridontal infection lead to acute endocarditis? Do you want to send the patient away untreated with a regimen of PCN-VK, trusting in PT compliance? I know of at least one medic who did just that...with dire consequences. It may be worth running labs before you let the patient start a week long regimen.
Also worth consideration is the typical stoicism of third world patients. I've seen teeth pulled just as mentioned in the instigative article, ie, sans anesthesia. These are all factors in your patient care decisions.
For the most part however, peridontal infections can be treated safely with PCN (or perhaps Cipro for those with allergies), then a return visit can allow you to remove the tooth with greater patient comfort.

[Sacamuelas]

Good post. A little background to let everyone know why this thread came about on Aprof.

This post was started to discuss the reasons behind and treatments for inadequate anesthesia in a severely infected local area. The original example was a severely abscessed tooth needing to be extracted. This process, however, is relevant to ANY area on the body that will need local anesthesia for debridement, treatment, etc. So this is relevant info for all.

Originally posted by troy2k
First, I will admit that I had terrible luck trying to find ANYTHING on this subject. However, here's what I've pieced together on the physiology of the subject.
There are 3 major features underlying inflammatory pain: a change in the peripheral sensitivity of high-threshold nociceptors--ie, increased sensitivity; an alteration in the chemical makeup of the neurons in the nervous system, a change in their properties and function-- called a phenotypic switch; and finally an increase in the excitability or the responsiveness of neurons within the central nervous system, and this represents central sensitization.

These are good explanations of the process that I had understood to describe the physiology behind increased sensitivity to stimulus in a chronic inflammation area. I.e.: a normally "non-threshold" level stimulus actually causing nerve discharge (reaching the threshold) due to physiological changes that led to increased "sensitivity" in the nerve bundle or CNS. This process is seen all over the body.. I.e.: a light touch on a "bruised" area causing the patient pain when that amount of pressure would never have caused a pain response w/o the prior inflammation in the area causing the changes you described.

That being said, these changes could be present in the original scenario in the mouth. A good review... but I don't think these side effects of inflammation are the cause of the lack of adequate anesthesia in an "infected" area. None of these things would cause a local anesthetic not to work as predicted.

Originally posted by troy2k
More importantly maybe is the proliferation of proteolytic substances, which may be responsible for the destruction (lysing) of opioid and amide receptor sites, inhibiting analgesic response.
As I said, at this point in time I found NO specific references to the phenomenon of decreased analgesia due to local infection. I have however researched this before. At that time there was little if any understanding as to the mechanisms involved. Much of this is still theory on my part, and I'd be glad to hear what others have found.

Not a proteolytic function..... good thinking though. That type of situation would not cause any of the common local anesthetics to cease working b/c they do not have "receptors" that can be blocked or destroyed. They work differently than opiod type analgesics. It is important to know how local works to understand why they don't work as well in infected environments. Anybody want to describe how local anesthetics block nerve transmission?

What happens to the local tissue environment in an infectious "abscess" or "cellulitis" situation? It isn't changes in the nerve that causes the anesthetic not to work in severely infected areas. The mechanism is well understood.... anyone else got any ideas?

Originally posted by troy2k
Now the important stuff: if you have a patient who falls into this category, it becomes a question of priorities. Will his peridontal infection lead to acute endocarditis? Do you want to send the patient away untreated with a regimen of PCN-VK, trusting in PT compliance? I know of at least one medic who did just that...with dire consequences. It may be worth running labs before you let the patient start a week long regimen.
Also worth consideration is the typical stoicism of third world patients. I've seen teeth pulled just as mentioned in the instigative article, ie, sans anesthesia. These are all factors in your patient care decisions.
For the most part however, peridontal infections can be treated safely with PCN (or perhaps Cipro for those with allergies), then a return visit can allow you to remove the tooth with greater patient comfort.

Will get to the rest of your post after we get through the cause for local anesthetic failure. Great post Troy. If you didn't know all the answers....trust me a LOT more people didn't either.

[troy2k]

I remember the last time I found a reference to this. It all but said "Hey we don't know how this happens, it just does." Of course that was 4 years ago.

[Eagle5US]

and I both posted the reason for Local Anesthetic failure in areas of infection...
Keep looking...it's out there

Eagle

[troy2k]

Performed 3 Searches, variations of Analgesia and Infection. No dice. I don't have 2 hours to look tonight however. Maybe later.

[Eagle5US]

May not necessarily be on THIS site...

Eagle

[NousDefionsDoc]

Originally posted by Eagle5US
May not necessarily be on THIS site...

Eagle

LOL - I don't think it was.

[Sacamuelas]

I think I partially covered it once on this site. I am going to search for it, cut/paste when I get a chance to save time.

Edited...couldn't find my previously typed answer on this site either, will look for it elsewhere and cut/paste/post when I find it. LOL

[Sacamuelas]

Large fluctuant abscesses are better treated with incision/drainage and Ab. If very swollen and fluctuant like in this case, a Penrose drain is sutured into the incision to allow longer and complete drainage. As to the previous question, I've never used a needle to aspirate/drain an area before (unless I thought I was facing a possible vascular tumor). In the field and in a situation where you would not feel comfortable or properly experienced to incise with a scalpel, a needle might be safer and would still get some benefit.

I usually use a #11 or 15 blade for incision, then blunt dissect/probe to obtain good access/drainage from the pocket. Incision does not have to be large at all esp. if a drain is placed.

If you are going to extract a tooth with a concurrent severe localized abscess present, you will most likely need to use high quantities of local and anesthetize the area by nerve blocks verses infiltration to get the anesthesia as far away from infected area as possible. Also, PDL injections (down the side of the tooth between the root and the bone) can be given to place anesthesia directly into the bone. They can be given and may be necessary even after a good nerve block administered.

Problems with inadequate anesthesia are caused due to the chemistry of the anesthetics themselves. The inflammatory/local infection process produces acidic products; the PH of normal tissue is 7.4; the ph of infected areas is 5 to 6.

The lower the ph of the area (more acidic it is) the higher the % of anesthetic that you inject is converted to the inactive form due to acid/base reactions. If you want more of a description, it is really boring tso be warned. It involves fun things like the Henderson-Hasselbach equation!!



I don't want to mislead you.... inactivated is really the wrong term but it defines its action.

The anesthetic when placed into solution in the syringe is actually found in equillibrium between its two forms.

• its "active" form- neutral charged (base form)
• its "inactive" form which is called positively charged (cation form.

Normally, a syringe of 2% lido 1:100,000 epi is buffered to be slightly alkalytic ( ph>7.0). This keeps a majority of the anesthetic in the solution in the "base" or active form.

Upon injection, which form the anesthetic takes is directly determined by the ph of the surrounding tissue it is injected into. So if the tissue environment is acidic (as in a severe localized infection) then a majority of the anesthetic immediately converts over to inactive “cation� form due to basic chemistry equilibrium principles.

The reason it is “inactive� is because it cannot diffuse across a nerve's membrane when its in the + charged “cation� form. Therefore, it is considered "inactive" as an anesthesia agent because it cannot get “in� to perform its function. More than that, and I am breaking out the equations and chemistry!! LOL

Hope that helps.... Glad I didn't have to retype all that. haha

so, all this talk about anesthesia and lidocaine...

how much lidocaine can you inject into the wound/tooth/etc of an average 70 kg man... if its

1% plain
1% with epinephrine...

why is there a difference?
what will be the first side effects you see if you give too much?

doc t.

[Sacamuelas]

My lido concentrations are 2%. Cartridges are 1.8 ml

It is available in:

• 2% Lido, no epi
• 2% Lido, 1:100,000 epi
• 2% Lido, 1:50,000 epi

How much can you give? what is limiting drug? what situations occur where the other drug is the limiting factor? How much can be safely given in those instances?