Oxygen: an unreliable friend, page 15   March 1 2010  -   The antioxidant prescription - excerpts    Bruce Wylde 


Your average well balanced  atom has a nucleus at the centre, and whizzing around the nucleus is the familiar cloud of electrons -just the right number of them. Under certain circumstances, however, atoms can lose an electron or two, and such atoms then wander around looking everywhere for replacement electrons attached to other atoms. There are the needful characters call radicals -  and sometimes free radicals. None of them are more reactive than the oxygen radicals. 

Apoptosis ( programmed cell death)

In 1961, Leonard Hayflick and Paul Moorhead, working at the Stanford University School of medicine, determined that normal cells can divide only a limited number of times, after which cells effectively commit suicide.  The number of times a cell is generically programmed to reproduce, dubbed the ‘‘hayflick limit’’, varies from species to species. In the case of human cells, the Hayflick limit is about fifty and is directly linked to the lifespan of individuals, Put bluntly, its’s difficult for you and me to live on when our cells are preprogrammed to conk out after so many recycles. Here, suggested Hayflick and Mooread, might be the truth about aging.

As work in this area progressed, it turned out that free radicals played a role in this programming, In fact, free radicals have turned out to be nature’s preferred mechanism of self-destruction when a cell’s time is up. The scientific name for this programmed death is ‘‘apoptosis’’.

Meanwhile the study of antioxidants has also moved forward.. Dr. Lester Packer, a senior scientist Lawrence Berkeley Laboratory, was among the first to describe the role of antioxidants in the health of organisms. He proposed that antioxidants function not singly but as a network to balance overall free radical activity. Packer demonstrated that antioxidants synergies with one another and, even more importantly, recycle one another. In order to neutralize free radicals antioxidants need to work like a team of firemen putting out a fire: some man the pumper truck, some are up the ladder, some are at the hose. Some move right in close to the fire to up out the flames, where others help the victims of smoke inhalation back away the fire. You can’t get away with sending only one antioxidant - say vitamin E - into the fray: that would be like having all the firemen rush to the end of the hose, with no one left to turn on the water. As you’ll learn later in this book, using single antioxidants in high doses can actually do you more harm than good. 

Dr. Packer has focused, rightly, on the synergy of antioxidants. He has described five pivotal antioxidants, which he calls network antioxidants: alpha-lipoid acid, coenzyme Q10, vitamine C, the naturally occurring forms of vitamin E, and glutathione. His conclusion; theres’a synergy between these antioxidants that slows aging and prevents and treats disease.  The clear  message that emerges from Packer,s review of the literature and from his own work is that antioxidants should be taken as a balanced network and at does specific to the individual case or condition. 

People who live to be 110 or older have higher levels of antioxidants in their bodies than less long-lived individuals. 

When stress is high for any prolonged period of time, the body breaks down rapidly and blood pressure can rise. High blood pressure and stress can push you over the boiling point. Free radicals are produced at alarming rates and they end up causing damage to artery linings. You’re on track for a heart attack. 

Adhesive Arachnoiditis is a chronic, insidious inflammatory reaction of the arachnoid matter of the spinal meninges and intrathecal neural elements that cause debilitating, intractable pain and a range of other neurological problems. It has been regarded as rare by the medical community, but the true scale of the problem remains unknown for a variety of reasons.

The sad fact is that adhesive arachnoiditis remains a contentious diagnosis, which may reflect the medical profession’s reluctance to acknowledge this largely iatrogenic condition.

Dr Sarah Andrea Smith -Fox, MBS, states: 



that the article's aim is to facilitate a clearer understanding of arachnoiditis for both patients and their physicians, so that they can work together to combat the devastating effect the condition can exert upon people’s lives.

Many medical practitioners regard arachnoiditis as a rare dinosaur, considering it related to oil-based myelogram dyes, which are no longer in use. This misconception underlies a general tendency to underestimate the ongoing impact of the condition. Far from being a historical curiosity, adhesive arachnoiditis is a ‘clear and present danger’ which needs to be addressed thoroughly in order to reduce its future impact.

Symptoms & Signs

  1. neuropathic pain, often non-dermatomal*; mostly lower limbs, low back but may also affect upper half of the body
  2. secondary musculoskeletal pain +/- fibromyalgic symptoms; joint pains; headaches
  3. bladder/bowel control dysfunction +/- sexual dysfunction
  4. motor weakness, cramps (tonic)
  5. profuse sweating/temperature control problems; CRPS type appearance.*

will include allodynia, dysaesthesia, bizarre sensations (walking on glass, water running down the leg) transient lancinating pains/electric shock sensations; sensory inattention etc. as per other types of neuropathic pain. CRPS may appear as altered skin colour, swelling, change in sweating, exquisite sensitivity, after minor injury.

The course of the condition is such that it tends to fluctuate, with intermittent flare-ups, but overall most patients will plateau out' and remain fairly stable unless there is an event such as a fall, accident or further surgery, which can cause a rapid deterioration.-Smith-Fox


Arachnoiditis most commonly arises from spinal surgery (especially multiple operations), severe trauma to the spine, myelographic agents, especially the older oil-based dyes, viral and bacterial meningitis, tuberculosis, syphilis, HIV, intrathecal hemorrhage, ischemia of the neural tissues, intraspinal injections of steroids, epidural and spinal anesthesia, multiple lumbar punctures,  and blood in the cerebral spinal fluid (CSF)due to subarachnoid hemorrhaging, epidural blood patch or trauma - Aldrete

Measuring the problem

Expert Dr. Charles Burton, of the Institute of Low Back and Neck Care, Minnesota, has written extensively about arachnoiditis, and (4) has attempted to suggest an estimated figure for cases in the US, using results of an international study that showed lumbo-sacral adhesive arachnoiditis to be responsible for abo ut 11% of all Failed Back Surgery Syndrome cases. Tying this in with the number of surgeries performed in the last 50 years, and an average rate of 25% FBSS, he estimates “at least 1,000,000 FBSS cases in the US would then have been causally and primarily due to the production of lumbo-sacral adhesive arachnoiditis. If one brings in the rest of the world the case estimate would have to be doubled.”

Dr. Burton also suggests that between 1940 and 1980 about 450,000 oil-based myelograms were performed in the US every year, giving a total of 19 million*, of which he estimates 5% sustained clinically significant adhesive arachnoiditis (although probably all had anatomical arachnoiditis) as a result, which gives a figure of 950,000 sufferers in the US alone.

Not only do I have the privilege of having administered an  intravenous infusion of lidocaine but I also, over the years, developed a formula to achieve relief and support the lidocaine treatment. 

You see, I am one of those patients who react very badly to prescribed medications such as anti-depressants, anti-psychotics, anti-epileptics, narcotics, opioids … For example, cymbalta, an anti-depressant that sent me to bed for one week, after ingesting one pill at a low dosage. Or Tramadol, a narcotic that sent me to the bowels of obsession after ingesting one pill. My brain felt like it was being taken over by the chemicals and frozen in place. One thought ran through my mind only:"I have to do myself in''  -   like a ticker tape, running so fast and furious. I could visualize the phrase going around and around. A very frightening experience, indeed. Opioids did help somewhat to lower the pain at a level of tolerance. Nevertheless, the chemicals were interfering with certain area of my brain. I am an artist, love doing portraits but under the influence of opioids, I could no longer capture the essence of a person on paper. I could no longer get the resemblance in place. You can see here the trial and errors of sketching a portrait and not succeeding while taking fentanyl and morphine. You can compare it to the finished portrait once I was receiving the lidocaine infusion after weaning myself off the opioids and narcotics. 

Over the years I have been asked what I do, in order to obtain relief. I have decided to share with you the information. From here, you can easily tweak and research what would be best for yourself if you are so inclined to do this. 

Here we go:

Natural supplements: 

MSM (sulfur) from the Flora company, the quality of its product is at its optimum.  I find it tames the burning, the muscle spasms, the deep aching within. In tough days I can ingest up to 6,ooo mg per day. 

Carnitine in powder. Very strong and effective anti oxidant against the pain.

Kelpasan from A.Vogel natural manufacturer of supplements. This is basically iodine in pills. It supports my thyroid gland. 

PGX - I am hypoglycaemic - Pgx helps control my blood sugar levels. It is also high in fibre, a bonus for the poop department. 

Vitamine C  occasionally only. If I find that I need an immune system booster to counteract some cold viruses. 

Tea tree oil(melaleuca)is a very powerful  natural antibiotic made from a tree in Australia. I use it for everything including ingesting few drops in water. Very efficient if you have an infection in a tooth, it helps with the pain and the infection.  For earaches, apply externally under the lobe of the ear, it also alleviate the pain and the infection. WebMD recommends that it is not safe to drink it. I don't agree, I have been ingesting this remedy, as needed, for years. It tastes awful! but it works and delivers its promises. 


for the pain:

lidocaine infusion:  Mild anesthetic administered intravenously to alleviate the pain. I am currently receiving 6mg on a monthly basis, with a saline solution. 

Ketamine   an anesthetic that I receive orally. I ingest 15 mg per day. I received 20 mg in an infusion along with lidocaine, 5mg. It was not effective for me in this form of administration. I have better results with the compounded ketamine taken orally. 

Ointment: composed of Ketoprofen/Gabapentin/lidocaine. this cream is compounded by a pharmacy. It is excellent for muscle spasms, ache, burning, electrical shock pain. It is a universal compound that all pharmacists have access to. 

Percocets:  This pill is split in quarters.  I detest the high that comes with ingesting a whole pill. I very rarely use this form of painkiller. During the summer, I might need one quarter  every other day. In wintertime, depending of the weather, I might take an average of ¾ of a percocet per day. 


DHEA: is a natural hormone that is secreted by our adrenals. As we age and reach menopause, the level declines. Corticosteroids and opiates deplete the level of DHEA. I ingest 25 mg per day. (on hold)


DIET: Very simple anti inflammatory diet.  

Beef is no longer part of my regular diet. Pork is never ingested, as it is the most contaminated meat on the market. Have you heard of tape worm? That is what pork brings you as a gift to your colon . 

Fish in abundance. Certified organic chicken is certainly welcome. 

No more pasta. Very little bread but if elected to eat it, it must be multiple grains. Absolutely no refined sugar. substitutes such as XYlotol, natural palm sugar, cane sugar, agape are safe if there is no excess. 

Fruits, vegetables, nuts, fibre in greater quantity.   


Health of colon

Cleansing every year. Fasting on fruits and veggies for 10 days is beneficial for a healthy colon. It also helps with the pain. Kefir and yoghurt are the favourite means of keeping regular bowel movements. 


How to Initiate and Monitor Infusional

Lidocaine for Severe and/or Neuropathic Pain

Rebecca Ferrini, MD, MPH, CMD, and Judith A. Paice, PhD, RN

Dr. Ferrini is Medical Director of Edgemoor Hospital, a long-term, 24-hour skilled nursing care facility operated by the County of San Diego in Santee, California.

Dr. Paice is Director of the Cancer Pain Program, Division of Hematology-Oncology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.

Case Report

The patient, a 51-year-old woman diagnosed with primitive neuroectodermal tumour (peripheral neuroendothelioma) 4 years prior, presented with severe (10/10) unrelenting neuropathic pain due to T6-T8 spinal-cord compression. Increasing doses of intravenous (IV) morphine up to 50 mg/h with frequent 25-mg boluses of morphine provided inadequate relief. Adjuvant analgesics, including gabapentin, baclofen, amitriptyline, clonidine, and clonazepam,provided little relief or caused significant side effects.

Because of the significant pain and lack of response to standard therapies for neuropathic pain, the decision was made to begin a trial of parenteral lidocaine. Treatment with 100 mg of lidocaine IV (approximately 1.5 mg/kg) over 20 minutes produced a rapid decrease in pain intensity over the course of the infusion. Because the trial was successful, a lidocaine infusion was

evere, intractable cancer pain is often due to neuropathic pain syndromes. Neuropathic pain can develop when nerves are injured, compressed, infiltrated, or affected by toxins, as commonly occurs in malignancies, as well as in HIV, diabetes, and other comorbidities common in people with cancer. Although opioids and adjuvant analgesics can be effective in most of these patients, a few individuals will continue to experience unmanageable pain. Novel techniques, such as parenteral lidocaine administration, are beginning to be used in the management of severe neuropathic pain.

Pathophysiology of Neuropathic Pain

To understand the rationale for using parenteral lidocaine, one must appreciate the underlying mechanism of neuropathic pain syndromes. However, because neuropathic pain syndromes represent a diverse group of conditions, one single mechanism cannot explain the underlying pathology. Changes can occur within the peripheral, central, and autonomic nervous system, and multiple

continued at 100 mg/h. Attempts to reduce the lidocaine infusion rate resulted in increased pain.

As this was a new therapy,we attempted a variety of delivery strategies. Continuous subcutaneous, continuous IV, IV bolus only, or a combination of continuous and bolus lidocaine were tried. The patient reported highest satisfaction with a continuous IV infusion accompanied by bolus doses as needed. As her pain was now better controlled, she was discharged home with hospice care after more than 3 months’ hospitalization.

Ongoing clinical monitoring and frequent dosage adjustments continued in the home setting. On average, adequate pain control was maintained with a lidocaine infusion rate of 10– 15 mg/h with a 25-mg bolus of lidocaine every 5 minutes for pain exacerbations. Four months after discharge, she died suddenly after development of superior vena cava syndrome [1].

mechanisms are likely involved. Within the peripheral nervous system, changes include abnormal nociceptor (small fibre neurons transmitting noxious stimuli) sensitization and ectopic impulse generation, leading to spontaneous discharge [2, 3]. The neuron becomes more sensitive to any stimulation, resulting in spontaneous pain and hyperalgesia (normally mild painful stimuli, such as a pin prick, are perceived as extremely painful).

Another hypothesized peripheral mechanism includes the development of ephaptic conduction between sensory neurons, where electrical currents in one neuron excite impulse activity in nearby neurons. Furthermore, neuropeptides, such as the cytokine tumour necrosis factor-α, are released in response to inflammation. These cytokines are believed to generate spontaneous ectopic activation of nociceptors [4]. Since conduction within neurons is mediated in part by changes in ion concentrations across the membrane, agents that block Na+ channels, such as the local anesthetics, are often used to relieve pain [5].

Sodium channel blocking agents, including systemic local anesthetics such as lidocaine, have long been used to treat acute pain and, more recently, chronic pain [6–9]. At subanesthetic doses, lidocaine blocks neuronal function in active or depolarized neurons without interfering with the normal function of other sensory or motor neurons [10]. Historically, outside of its use for procedural pain, parenteral lidocaine has been used as a “challenge” to elucidate whether the patient has neuropathic pain and to ascertain whether adjuvant therapy using oral analogs of lidocaine, such as mexiletine, might be effective. Several open label trials report the benefit of short-term intravenous (IV) lidocaine infusions, lasting 45 minutes to 1 hour, in a variety of neuropathic pain states, including postherpetic and diabetic neuropathy [9, 11, 12]. Anecdotal reports suggest that some patients obtain sustained relief, although many patients report that the pain returns hours or days after the infusion is discontinued.

Based upon these experiences, and the prevalence of severe neuropathic pain in our hospice, we explored the prolonged use of IV or subcutaneous (SC) lidocaine infusions to treat both neuropathic and mixed (neuropathic and nociceptive) pain syndromes.

Initial Experience

While working at an inpatient hospice in 1996, one of us (R.F.) began treating patients suffering from severe neuropathic pain with parenteral lidocaine infusions. At first, we regarded lidocaine as too dangerous for use except by anesthesiologists. Therefore, we investigated lidocaine therapy only in the most difficult-to-treat pain states, restricting its use to only those patients who were closest to death and who might be willing to accept the risk of this “unconventional and possibly dangerous therapy” (as we explained it). However, as our team developed more experience, we came to see lidocaine’s effectiveness, both in controlling patients’ pain and improving their quality of life. Furthermore, despite our fears, we observed little toxicity as an effect of this drug. We have found parenteral lidocaine to be effective in those with chronic neuropathic pain, particularly when it was associated with malignancy, as well as for severe pain of other aetiologies. We have now treated over 100 patients using this technique, some for weeks or months, and have identified advantages to this therapy, as well as characterized those patients who might benefit most from it.


Advantages of Lidocaine Therapy

Lidocaine is inexpensive and effective. Adverse effects of sedation, confusion, nausea, and constipation that accompany the use of opioids and other analgesics, tend to occur less frequently with lidocaine therapy. The side-effect profile of parenteral lidocaine delivered by infusion is predictable and has a wide safety margin [4]. Thanks to its short half-life, the symptoms of lidocaine toxicity are transient and easily reversible by lowering the infusion rate.


Who Might Benefit From Lidocaine

Infusion Therapy?

Parenteral lidocaine has been reported to be effective in small studies of various neuropathic pain conditions, including diabetic neuropathy, postoperative pain, post-herpetic neuralgia, centrally mediated pain, headache, and malignant nerve infiltration [13–20]. Based upon the experience of R.F. with more than 100 patients, many or all of whom whereas receiving opioids, infusional lidocaine is effective when treating visceral or central pain. Parenteral lidocaine may also be useful when opioids are ineffective or causing unacceptable adverse effects.


To determine whether the patient is a candidate for parenteral lidocaine infusion, a thorough pain assessment is critical. Patients should undergo complete pain history, quantitative pain assessment, and physical examination. Prior adjuvant therapy and allergies to “caine” anesthetics must be elicited. The presence of heart failure or liver disease, which would increase the toxicity of lidocaine, must be ascertained. A complete medication history is essential, as adjuvant therapies and other, less-invasive modalities are warranted prior to beginning parenteral lidocaine.


The purpose of a lidocaine challenge is to assess whether an individual patient’s pain is responsive to lidocaine and whether the patient can tolerate the medication. The dosage for testing purposes infusional Lidocaine generally 1–3 mg/kg (100 mg is often used) administered IV in a concentration of 8 mg/mL over 20–30 minutes. During the bolus infusion, careful clinical observations of vital signs and pain intensity are conducted at least every 15 minutes. If SC administration is preferred, the initial loading dose is administered over a longer period (30 minutes to 1 hour), and response is generally delayed. If SC infusion is elected, lidocaine is easily concentrated at 40 mg/mL, allowing a 2–3 cc initial dose and hourly infusion rate of 2–3 cc/h. If ineffective, the lidocaine challenge is discontinued and other pain relief modalities must be selected. If effective, an infusion is started.

Lidocaine Infusions

If the lidocaine challenge is effective or partially effective, the patient is started on a continuous infusion, either SC or IV, at 0.5–2 mg/kg per hour, using the lowest possible dose that controls the pain (Table 1). Although lidocaine is generally given as a continuous infusion for pain, we have also tried a patient-controlled analgesia (PCA) format in which the patient could self-administer bolus doses in some cases of intermittent, severe pain.

Lidocaine infusions may reduce pain dramatically or subtly. 

Table 1

When Lidocaine Challenge Works, What Next?


Gradually titrate downward to try to determine the lowest possible effective dose of lidocaine.

Monitor for any signs of toxicity, particularly after dosage increases.

Reduce opioids rapidly if patient demonstrates signs/symptoms of toxicity (particularly sedation).

If pain is exclusively intermittent, initiate a trial of bolus administration.

If the patient did not receive an adequate trial of adjuvant analgesics, sequentially try adjuvant therapy and titrate the dose upward until analgesia or adverse effects occur.

Discuss signs and symptoms of possible toxicity with patients and families.

Assess the competency of the caregiving situation if unable to wean the patient off lidocaine and he or she wishes to return home.

If lidocaine infusion continues to be indicated:

Consider invasive therapies, such as epidural nerve blocks.

Consider home infusion.

 patients will report dramatic stepwise “erasing” of their pain. In other cases, however, patients might say the pain is still severe (rating it a “10” on a scale of 0 to 10) but more “bearable.” Another indication that lidocaine is effective is an improvement in the patient’s functional status (eg, a patient who could not walk due to pain begins to walk) or a reduction in opioid use. Or patients may say, “I don’t feel it working,” but when the rate of infusion is reduced, the pain returns and they notice its previous effectiveness.


As with any therapy, the ideal is to use the lowest effective dose of medication to treat the patient. The usual method of establishing the lowest effective dose is to reduce the dose of lidocaine gradually until pain returns. Doses above 2 mg/kg per hour are rarely indicated. This experience with parenteral lidocaine mirrors that of Wallace and colleagues [8], who reported a lidocaine dose-response curve for pain relief characterized by a clearly defined breakpoint in dosage, below which pain persisted and at or above which pain was dramatically reduced. Although doses may be reduced among those with hepatic or cardiac disease, these conditions are not contraindications in the case of severe neuropathic pain.


Lidocaine infusions to manage pain are generally in the range of 1–2 mg/kg per hour. At this rate, blood levels are often less than 3 µg/mL and toxicity rarely develops. If blood levels increase, the side effects are sequential, relatively predictable, and easily reversed by stopping or slowing the infusion [4]. At blood levels of 4–6 µg/mL, patients may complain of lightheadedness, numbness around the tongue or mouth, and/or dizziness. They may note a metallic taste in their mouths or experience an increase in blood pressure. The infusion should be slowed or stopped if any one of these events occurs. Although we initially drew blood to measure plasma levels of lidocaine when using this drug for analgesia, this level of monitoring does not seem to be necessary in a palliative care population, nor do most patients want venipuncture.

Plasma concentrations of lidocaine rarely, if ever, exceed these levels when infusions are used for pain. To provide a reference for lidocaine effects at higher plasma levels, at approximately 8 µg/mL, patients can experience visual or auditory disturbances, dissociation, muscle twitching, and decreased blood pressure. At 12 µg/mL, convulsions may be noted; at 16 µg/mL, coma may ensue, and at levels above 20 µg/mL respiratory arrest and cardiovascular collapse can occur. Thus, at the doses used to provide pain relief, parenteral lidocaine infusions are safe.

Other toxicities include local redness or erythema at the SC infusion site. Changing the site every few days can obviate the local irritation.

Titrating Opioids With Lidocaine

Many patients whom we have treated with lidocaine infusions were receiving high doses of parenteral or oral opioids concomitantly. Lidocaine infusions can reduce pain and the need for opioids dramatically. In fact, if opioid dosages are not reduced when pain reduction is achieved through a lidocaine infusion, opioid side effects may develop or worsen.

For example, a previously well-tolerated opioid dose may lead to significant sedation when pain is relieved by infusing lidocaine. Interestingly, we have never seen any sign of opioid withdrawal, despite rapid discontinuation of even high-dose opioid therapy (eg, a reduction from 500 µg/h of SC fentanyl to no opioid use over 24 hours or 90 mg/h of IV hydromorphone titrated to 1–2 mg/h in less than 24 hours).

Adjuvant Therapies

In an ideal world, oral adjuvant therapies would already have been tried prior to instituting a parenteral lidocaine infusion, but some patients may present with severe neuropathic pain without ever having had an adjuvant analgesic. Most adjuvant analgesics must be titrated gradually, delaying pain relief. Ideally, parenteral lidocaine is a time-limited strategy for rapidly treating severe neuropathic pain. Once pain is under control, adjuvant therapy can be instituted and titrated so that the pain can be managed more conveniently, without the need for catheters or infusion pumps.

However, despite a wide variety of adjuvant agents, including antidepressants, anticonvulsants, corticosteroids, and antiarrhythmics, very little information exists regarding which therapies might be most effective in those patients who have responded favourably to lidocaine infusions. The majority of the patients we treated with parenteral lidocaine therapy were successfully transferred to


Lidocaine Infusion


Your doctor has prescribed lidocaine to treat your pain. Lidocaine is a local anesthetic similar to the anesthetic dentists use to numb your tooth when you get a filling. It seems to work by quieting nerves, which are firing when they shouldn’t be, thereby reducing your pain.

Lidocaine belongs to an entirely different family from morphine and can be extremely effective at reducing certain kinds of pain. Lidocaine is administered either intravenously (in the vein) or subcutaneously (under the skin) by a portable pump. The pump delivers this medication as a continuous infusion, delivering the same amount every hour for 24 hours a day. In some cases, your pump may allow you to receive extra doses, called bolus doses, which you can give to yourself if the pain returns.

Side Effects of Lidocaine

Lidocaine is a relatively safe drug when given in low doses. However, even at low doses, certain side effects can occur. The most serious side effect is an allergic reaction to the medication, which can produce sudden, severe difficulty in breathing. The allergic reaction also can increase the chances of having an irregular heartbeat, which, in rare cases, can lead to sudden death. Although allergic reactions to lidocaine are serious, they are fortunately rare.

The most common side effects you might experience are usually related to having too much of the drug in your body. When this happens, you may experience numbness around your mouth, dizziness, or even a sense of being drunk, perhaps with slurring of speech.

You also may experience hallucinations, muscle twitches, or even a sense of being detached from your body. Though these side effects go away very quickly, once the infusion is stopped or lowered and blood levels of lidocaine drop, they should prompt a call to your nurse.

In rare cases, lidocaine can produce seizures, usually when the dose being given is too high. In these cases, the infusion should be stopped, the nurse called, and seizure medication given.

Sometimes, you may experience problems in the area where the lidocaine enters the body. If the medication is given under the skin, you and the nurse should check for redness, soreness, or hardening of the site. These signs indicate that the site should be changed. In general, the site should be changed every 3 days. However, if redness develops, the site of entry may have to be changed more frequently.


Ferrini Paice

Table 2

Protocol for Home Infusion

Determine whether to use:

Subcutaneous or intravenous administration.

Bolus doses only, continuous infusions, or a combination of both.

Patient must have a stable caregiver situation, with 24-hour supervision by a competent adult.

Home Infusion of Lidocaine

If the patient is unable to taper off the lidocaine, refuses or is not a candidate for more invasive therapies, and requires continuous infusion at home for ongoing pain relief and, moreover, strongly desires discharge, home infusion may be considered (Table 2). Lidocaine infusions may be administered

Patient must consent to being visited by a registered nurse 2–7 times a week. at home via an ambulatory pump identical to those

Patients should understand that any redness or induration at the site of subcutaneous injection indicates a need to switch to a different site (abdominal and thigh sites are preferable).

Patient should agree to frequent adjustments of lidocaine dosage in an attempt to determine the minimum dose at which patient is comfortable.

Patient/caregiver should have the ability to clearly describe signs and symptoms of lidocaine toxicity and show ability to turn off the pump.

Patient/caregiver should be provided with a lidocaine patient information sheet.

used for opioid infusions in a PCA setting. Because they are compatible, lidocaine may be used together with opioid infusions. Another advantage is that lidocaine is inexpensive, with a 24-hour supply costing less than $5.

Lessons Learned

Consider providing benzodiazepine in home for sublingual or subcutaneous administration in the event of seizures.

oral agents, most commonly gabapentin. Because

Infusional few data exist, the clinician must use a trial-and error approach, sequentially introducing different


adjuvant agents and titrating each one until an analgesic or adverse effect occurs. If an adjuvant drug is found to be effective, the lidocaine infusion is gradually reduced and discontinued, if possible. If these attempts fail, patients may be maintained for weeks to months on infusional lidocaine without any adverse effects.

Lidocaine infusions, used over the short or long term, have become an indispensable part of the armamentarium for treating intractable severe pain, particularly neuropathic pain. Regardless of the setting in which lidocaine will be used, the interdisciplinary team must work together to educate themselves about this approach and develop policies and systems for providing this technique in a safe and timely manner. Finally, this modality deserves further study in the hospice and palliative care setting to determine the appropriate dose, schedule, route, and indications for lidocaine infusions to improve comfort at the end of life.


Ferrini RL. Infusional lidocaine for terminal

ly ill patients with intractable pain continued at home. Palliat Med 2000;3: 93–201.

Serra J, Ochoa J, Campero M. Human stud

ies of nociceptors in neuropathic pain. In: Hans-son PT, Fields HL, Hill RG, Marchettini P, eds. Neu

ropathic Pain: Pathophysiology and Treatment, Progress in Pain Research and Management. Vol

21. Seattle, Wash: IASP Press; 2001:63–83.

Baron R. Peripheral neuropathic pain: from mechanisms to symptoms. Clin J Pain 2000;16: S12–S20.

Mao J, Chen LL. Systemic lidocaine for neu

ropathic pain relief. Pain 2000;87:7–17.

5.Tanelian DL, Brose WG.Neuropathic pain can be relieved by drugs that are use-dependent sodium channel blockers: lidocaine,carbamazepine and mexiletine. Anesthesiology 1991;74:949–


Dejgard A, Petersen P, Kastrup J: Mexiletine for treatment of chronic painful diabetic neurop

athy. Lancet 1988;1:9–11.

Bach FW, Jensen TS, Kastrup J, et al:The effect of intravenous lidocaine on nociceptive process

ing in diabetic neuropathy. Pain 1990;40:29–34.

Wallace MS,Dyck JB,Rossi SS,Yaksh TL.Com

puter-controlled lidocaine infusion for the eval

uation of neuropathic pain after peripheral nerve injury. Pain 1996;66:69–77.

Rowbotham MC, Reisner-Keller L, Fields HL. Both intravenous lidocaine and morphine reduce the pain of post-herpetic neuralgia. Neurology 1991;41:1024–1028.

Tanelian DL, Victory RA. Sodium channel-blocking agents: their use in neuropathic pain conditions. Pain Forum 1995;4:75–80.

Galer BS, Miller KV, Rowbotham MC. Re

sponse to intravenous lidocaine infusion differs based on clinical diagnosis and site of nervous system injury. Neurology 1993; 43:1233–1235.

Ferrante FM, Paggioli J, Cherukuri S, et al. The analgesic response to intravenous lidocaine in the treatment of neuropathic pain. Anesth Analg 1996;82:91–97.

Marchettini P, Lacerenza M, Marangoni C, et al. Lidocaine test in neuralgia. Pain 1992;48: 377–382.

Edmondson EA, Simpson Jr RK, Stubler DK, Beric A. Systemic lidocaine therapy for post-stroke pain. South Med J 1993;86:1093–1096.

Brose WG, Cousins MJ. Subcutaneous lidocaine for treatment of neuropathic cancer pain. Pain 1991;45:145–148.

Shwager HA, Floyd RA, Ivey JR, et al. Phar

macodynamic modeling of pain response with chronic subcutaneous high concentration lidocaine in the treatment of sympathetically mediated pain. In: Proceedings of the 14th An

nual Scientific Meeting of the American Pain So

ciety; November 1995; Los Angeles, Calif.

Linchitz RM, Raheb JC. Subcutaneous in

fusion of lidocaine provides effective pain relief for CRPS patients. Clin J Pain 1999;15:67–72.

Baranowski AP, De Courcey J, Bonelo E. A trial of intravenous lidocaine on the pain and al

lodynia of post-herpetic neuralgia. J Pain Symp

tom Manage 1999;17:429–433.

Wu CL, Tella P, Staats PS, et al. Analgesic effects of intravenous lidocaine and morphine on postamputation pain: a randomized, double-blind, active placebo-controlled cross-over trial. Anesthesiology 2002;96:841–848.

Hand PJ, Stark RJ. Intravenous lignocaine infusions for severe chronic daily headache. Med J Aust 2000;174:157–159.


Correspondence to: Rebecca Ferrini, MD MPH, CMD (Certified Medical Director), Medical Director, Edgemoor Hospital, County of San Diego, 9065 Edgemoor Drive, Santee, CA 92071; telephone: (619) 956-2852; e-mail: rebecca.ferrini @sdcounty.ca.gov.

J Support Oncol 2004;2:90–94 © 2004 BioLink Communications



Go to top