Breastfeeding - my experience

Those that know me know that I am still feeding my almost three year old daughter and those that don't know this about me, may be surprised to know this. I feel passionate about breastfeeding and I know a lot about breastfeeding, positive and negative. Anyway I felt it was time to talk a little bit about my experiences, my opinions and my expectations; and I will say now that some of what I say may surprise you.

My Experience

When I fell pregnant with my first daughter and thought about how I planned to feed her, I merely thought "well I'll give breastfeeding a go but if it doesn't work out then I'm not going to beat myself up over it"....and I don't think that's a rare way to feel at all. I went to my antenatal class about feeding and noticed that there was a distinct drop in numbers attending. I listened dutifully to all the benefits to me and the baby and felt no real difference, and certainly no more prepared. I don't recall them discussing problems at all, though it is possible they did.

When my daughter was born, we did have skin-to-skin but in the immediate time following the birth there was no mention of feeding her. I certainly didn't have a clue what to do, or whether I should be trying to feed her or not. Anyway eventually someone did come to try and help me to breastfeed, I have no idea whether or not she was a midwife or maternity support worker. She certainly did her best, but my boobs would challenge most I think, as they are on the large side. Anyway she did manage to get her latched on but she didn't feed for long, and just wanted to sleep. Overnight she was very unsettled and I did my best to feed her but had no idea whether or not I was doing it right and come the morning I asked the midwives for some support. They did their best but she just didn't want to feed at the time they were able to help me, and when she did feed it was only for about 5 minutes. The midwives in the morning wanted me to stay a bit longer and get some more support with feeding, the afternoon midwives discharged me home. Did I feel confident? No, but having said that, I wanted to go home because I didn't feel that I was getting the support I needed whilst I was there anyway.

Over the next few days I gradually got sorer and my nipples cracked and were bleeding. I dreaded every single feed. However if someone suggested I switch to formula, I was like a stubborn child, I dug my heels in and was determined that it wasn't going to beat me. It was at this time, I actually discovered how much being able to breastfeed, mattered to me. I couldn't tell you why it mattered all I know is that it did. At that moment I certainly didn't give a monkey's about the health benefits, and I certainly wasn't thinking that formula was evil; I just knew that I wanted to breastfeed. Even now I can remember how determined I was whilst at the same time, I sobbed through every feed, and curled my toes.

Before I scare anyone who hasn't had children off breastfeeding for life....I would like to add that it changed very quickly - once I got the right support. I've actually already mentioned the inspirational midwife Annie who corrected my positioning and helped me on the road to pain free feeding. I saw Annie at home on day 5, and attended the breastfeeding group the same day. By the time I returned to the group a week later, the pain was gone. With my eldest daughter I went on to be pain free for the remainder of our breastfeeding journey which was ended by her when she was 13 months 1 week old. I attended the breastfeeding support group every week.....ok I wasn't experiencing pain but I did feel like I needed support. I made a lot of friends at that group, some of whom I consider amongst my closest friends now, one of which is in fact my second daughter's godmother. Having friends that had experienced the growth spurts, the distracted nursing child, the sleepless nights was essential.  Of course some of things are nothing to do with breastfeeding, but neither were the conversations about our husbands or families! The point was, someone had always had the same or similar experience and it meant you didn't feel quite as alone. At the time I was grieving the loss of my brother, who had died when my eldest was 10 weeks old; and whilst many of them may not have known that, they helped me more than they could ever know.


With my second daughter, I didn't anticipate any problems - after all, I had attended the group for well over a year, I'd already breastfed one child, I knew about all the problems to look out for...what could go wrong? Well...my daughter hadn't done all those things and she needed to learn how to feed, even if I didn't. There were no major problems, but boy did she have a strong suck on her and I experienced a couple of days of soreness as a result. When she was weighed on day 5, she'd already gained 13 ounces, so there was nothing wrong with her latch.

Over the coming months we experienced reflux , breast refusal, biting, mastitis and even a fairly long period of time where she would only feed from one side. I still have no idea why she only fed from one side; there seemed to be no real reason to it. She'd refuse to feed completely when she was teething but we invested in an amber teething necklace which seemed to do the trick. I was once a sceptic when it came to these alternative methods but the one and only other time she refused to feed, my husband had forgotten to put her necklace back on after her bath. The group helped support me, in that I knew it was quite common for babies to refuse to feed when they were teething, and that it was normal for different babies to react in different ways. With my first daughter, we'd never known she was teething, we'd just suddenly realise she had a new tooth.

When people found out that I had breastfed babies with teeth, they would always ask me about biting and doesn't it hurt. I have been bitten, and in all honesty, my second daughter once bit me so hard it drew blood. Not once did it occur to me, to stop breastfeeding because of it. I dealt with it in the same way I dealt with it any time she did something naughty. I told her very firmly no, and put her on the floor. She'd yell and cry, and I'd pick her up, tell her firmly not to bite and we'd continue. I'd like to say I only had to tell her once but it wouldn't be true. However I also learnt the signals for when she was considering biting, and the continued consistent reaction from me, ensured that it was soon a thing of the past; and she certainly never once bit me as hard again.


The couple of times I had mastitis, I was lucky in that I knew the signals and I was able to beat it becoming a more serious issue by feeding, feeding and feeding some more. I'd use a variety of positions to ensure that all the ducts were emptied properly. Again I am grateful to my attendance at the group, for knowing just how to handle it.

If you've learnt anything from this blog post, you should have worked out just how much I value the breastfeeding support group; it should therefore come as no surprise that I went on to become a breastfeeding mother helper and along with a friend, facilitated the group. I was awaiting training to become a peer supporter but I actually got my place at University before that happened. I did however attend the monthly training meetings with other mother helpers and peer supporters so I gained a wealth of knowledge about how to support women.

You might think from this blog post that I believe every woman should breastfeed...well you'd be wrong but I shall save telling you all about my opinion for my next blog post......

Inspirational Midwives

I have heard it said that along the way in my training it is likely I will see some bad practice, some ways of practising that I won't want to use and hopefully a lot of good practise. So it got me to thinking about putting down in writing what it was about the two midwives that I know, that inspired me so much, so that when I am suffering from a lack of confidence I can look back and read it. Of course it will be hard to convey exactly why they are so inspiring in writing but I shall do my very best. Those that know me and are local to me will know exactly who I am talking about but obviously I need to keep this confidential so I shan't be mentioning their names - I shall call them Jo and Annie for the purpose of this post.

I first met Annie when my eldest daughter was about 5 days old. She visited me at home to perform her heel prick test and she unfortunately had to come back and repeat it when she was 9 days old as she just hadn't bled well enough. I opened the door to her and cried with relief at seeing her. Now I shall talk in more detail about breastfeeding later but on day 9, I was at the end of my tether with breastfeeding. I was sore, my nipples were cracked and bleeding, I was incredibly engorged and I had a baby that wanted to be constantly feeding. Annie helped me to get her latched properly, and encouraged me to attend the breastfeeding support group later on that day. So later on that day I managed, somehow, to get myself out the door and down to the group. I shan't bang on about the group now, as I will cover it in more detail when I talk about breastfeeding, but Annie ran this group so amazingly well. She'd manage to balance supporting women, without ever judging them or pressuring them. She knew when it would help for someone to have a peer supporter provide one on one support and when someone needed more. When Annie ran the group we had a thriving membership, sometimes there weren't enough chairs; yet when government funding was pulled back, it meant she was only able to drop in on the group when she could, and the running of the group fell to the peer supporters themselves. Whilst the peer supporters did a fantastic job, the membership dwindled considerably. It was down to Annie and that group that led me to breastfeed as long as I did, as well as myself of course.

I can't remember when exactly I first met Jo as she'd sometimes come along to the breastfeeding group, though that was more Annie's domain, or whether or not it was at the  Baby Massage class that she ran. Jo has a wealth of knowledge on many many subjects not just midwifery related and I believe she has recently completed her Masters.

Together Jo and Annie ran the antenatal group/drop in. They were much like the antenatal classes run by the hospitals in some ways but far far better. They would cover all the usual topics you'd expect at, such as pain relief, positions in labour, instrumental deliveries, episiotomies etc. However what made this group so fantastic is that there was no limit on how often you attended. When I fell pregnant with my second daughter, I attended early on following some bleeding I had and then more regularly from around 28 weeks. It meant that you got to know the others that attended, some would be further along than you, and some would be earlier in pregnancy. When I attended the hospital classes when I was pregnant with my first daughter, we had one of those awkward get to know each other games and everyone was uncomfortable. At drop-in, as I shall call it, we did always introduce ourselves and although it was always a little bit uncomfortable, it got it over and done with, not to mention once you'd been a few times you found it easy. It also gave you a chance to say what had been going on with you that week, to raise something that might be worrying you, to moan about work or relatives. And it always felt like someone else had been through the same or was currently experiencing the same and that made for a very reassuring environment. So Annie and Jo provided this opportunity to access the information we needed, time to speak to a midwife but also time to speak with our peers. Separately they are both brilliant but together they are the best!

When I fell pregnant with my second daughter it was only natural to me to book with Annie. I saw her every week at the breastfeeding group and I felt so comfortable with her. Throughout my pregnancy I saw either Annie or Jo and got to know them both so much more. They gave me the confidence and the information to choose a home water birth. It was the ultimate joy when it was Annie and Jo that were present for the birth of my 2nd born. My first daughter was delivered by the midwives, my second daughter was delivered by me. Annie and Jo helped that to happen and in the case of a normal birth, this is how it should happen. The best part of this is, it's not only me they have this effect on. Amongst my friends, I can see how many they have empowered in their births....whether they were home births, Cesarean sections, instrumental deliveries or inductions....Annie and Jo inspired them all.

If I can be half as good a midwife as either of them, I shall be proud. I feel honoured to have known them, and words can't describe how I lucky I feel to have had them at the birth of my second daughter.

An unexpected pain

Anyone who has lost someone they love will know what I mean when I talk about the occasions where it hits you smack in the chest with a reminder of who you have lost, completely unexpectedly. There are of course the days that you know will be more difficult; the anniversaries, the birthdays, special occasions. You also know sometimes from the moment you wake up, that today is going to be a bad day, where the ache of missing them is as bad as the day you lost them. People tell you it gets better with time and that is both true and a lie. It's true that the fog lifts, and you are more able to function with every day that passes. However it's a lie that the pain lessens....at least that is the case for me.

I feel like I've started this post a little back to front as I am sure I have readers that don't know my history. My brother died in May 2006. He had a brain tumour that he just couldn't beat, despite his very best efforts. In spite of the fact that he'd been ill for some time, and we'd been told there was no more they could do, it still hit like a sledge hammer when he died. His wife had given birth to their son just two days previously, whom he sadly never met and it felt incredibly unfair. At the time, my eldest daughter was just 10 weeks old, and my sister's youngest son was just 8 months old so I don't know whether or not that made it feel worse to us, that he never got to meet his son. I have a very treasured photo of my brother holding my daughter but at the same time I almost feel guilty about having it at all. I could talk on and on about my brother - about his qualities and his faults but suffice to say I miss him just as much today as I did on the day he died.

Today at Uni I had one of those sledgehammer moments where the pain hit me hard in the chest completely unexpectedly. We were sat in our Ethics seminar talking about ethical decisions and one of the topics under debate was the case of Diane Blood who went to court to fight for the right to use her deceased husband's frozen sperm in order to conceive. The issue of consent was discussed and the fact that her late husband had not given consent for his sperm to be used if he should die but he also hasn't specified that he wouldn't want it to be used. When my brother was first diagnosed with a brain tumour and he and his wife knew that he was going to have chemotherapy, they made the decision to freeze some of his sperm knowing that they were planning to have a family. It is now an automatic part of the "service" to ask whether or not consent is given for the sperm to be used in the event that they pass away. My brother has given permission for it to be used so my sister-in-law will never have to fight for her rights there. However there are still a number of issues surrounding her actually using it so I know that it will never be an easy nor straightforward decision for her.

Anyway sitting in class today and listening to these debates going on around me on this topic; the rights of the deceased husband's parents, the rights of the children, the rights of Diane Blood. It hit me bang in the chest, that it could easily have been a conversation about my brother and his wife. Due to the fact that I didn't know my fellow students before beginning the course, they of course had no idea about my brother. Actually come to think of it, I don't think many people know about his frozen sperm....and why would they? Is it anything to do with anyone else?

It's made me think about my brother obviously but it's also made me think about the fact that we all bring our own histories and it isn't always obvious what someone has experienced. I believe that no-one should be taken at face value and that our experiences shape us and our opinions on things. Sometimes it is good to challenge yourself and think about why you think what you do? Where has it come from? If you explore it more deeply, is it what you truly think? Just to put this into perspective; I grew up believing that all terminations were wrong. I had never really thought about why I felt like this - was it my upbringing, my religion, how I really felt? Ultimately of course, I can only make a decision about what is right for me, and as a midwife, I need to be able to support women in their decisions without judgement. Therefore how I feel is somewhat irrelevant, providing it doesn't affect the care that I give. And that goes for anything not just terminations.

I feel a little like I have rambled my way through this post but I would like to share this very precious photo of my brother David, holding my daughter.

Pain Treatment with anti pain drugs

ACUTE PAIN

Sometimes treating the underlying condition doesn't immediately relieve pain even though the ideal treatment for any pain is to remove the cause, thus diagnosis should always precede treatment planning. Furthermore, some conditions are so painful that rapid and effective analgesia is essential (for example, the postoperative state, burns, trauma, cancer, sickle cell crisis). Analgesic medications are a first line of treatment in these cases, and all practitioners should be familiar with their use.


Aspirin, Acetaminophen, and Nonsteroidal Anti-Inflammatory Agents (NSAIDS) are drugs that considered together because they are used for similar problems and may have a similar mechanism of action . All these compounds inhibit cyclooxygenase (COX), and, except for acetaminophen, all have anti-inflammatory actions, especially at higher dosages. They are particularly effective for mild to moderate headache and for pain of musculoskeletal origin. Since they are effective for these common types of pain and are available without prescription, COX inhibitors are by far the most commonly used analgesics. They are absorbed well from the gastrointestinal tract and, with occasional use, side effects are minimal. With chronic use, gastric irritation is a common side effect of aspirin and NSAIDs and is the problem that most frequently limits the dose that can be given. Gastric irritation is most severe with aspirin, which may cause erosion of the gastric mucosa, and because aspirin irreversibly acetylates platelets and thereby interferes with coagulation of the blood, gastrointestinal bleeding is a risk. The NSAIDs are less prob lematic, but their risk in this regard is still significant. In addition to their well known gastrointestinal toxicity, nephrotoxicity is a significant problem for patients using NSAIDs on a chronic basis, and patients at risk for renal insufficiency should be monitored closely. NSAIDs also cause an increase in blood pressure in a significant number of individuals.


Treatment with NSAIDs in long-term therapy requires regular blood pressure monitoring and treatment if necessary. Although toxic to the liver when taken in a high dose, acetaminophen rarely produces gastric irritation and does not interfere with platelet function. The introduction of a parenteral form of NSAID, ketorolac, extends the usefulness of this class of compounds in the management of acute severe pain. Ketorolac is sufficiently potent and rapid in onset to supplant opioids for many patients with acute severe headache and musculoskeletal pain.


There are two major classes of COX: COX-1 is constitutively expressed and COX-2 is induced in the inflammatory state. COX-2-selective drugs have moderate analgesic potency and produce less gastric irritation than the nonselective COX inhibitors. It is not yet clear whether the use of COX-2 selective drugs is associated with a lower risk of nephrotoxicity compared to nonselective NSAIDs. On the other hand, COX-2-selective drugs offer a significant benefit in the management of acute postoperative pain because they do not affect blood coagulation. This is a situation in which the nonselective COX inhibitors would be contraindicated because they impair platelet-mediated blood clotting and are thus associated with increased bleeding at the operative site. A corollary of this is that COX-2 drugs do not provide the same degree of protection from thromboembolic cardiovascular adverse events such as myocardial infarction. In fact, in patients treated for arthritis, those treated with naproxen had significantly fewer adverse thromboembolic events than those treated with rofecoxib, a selective COX-2 inhibitor.


Opioid Analgesics Opioids are the most potent pain-relieving drugs currently available. Furthermore, of all analgesics, they have the broadest range of efficacy, providing the most reliable and effective method for rapid pain relief. Although side effects are common, they are usually not serious except for respiratory depression and can be reversed rapidly with the narcotic antagonist naloxone. The physician should not hesitate to use opioid analgesics in patients with acute severe pain. Table 11-1 lists the most commonly used opioid analgesics. Opioids produce analgesia by actions in the central nervous system. They activate pain-inhibitory neurons and directly inhibit pain-transmission neurons. Most of the commercially available opioid analgesics act at the same opioid receptor (mu receptor), differing mainly in potency, speed of onset, duration of action, and optimal route of administration. Although the dose-related side effects (sedation, respiratory depression, pruritus, constipation) are similar among the different opioids, some side effects are due to accumulation of nonopioid metabolites that are unique to individual drugs. One striking example of this is normeperidine, a metabolite of meperidine. Normeperidine produces hyperexcitability and seizures that are not reversible with naloxone. Normeperidine accumulation is increased in patients with renal failure. The most rapid relief with opioids is obtained by intravenous administration; relief with oral administration is significantly slower.


Common acute side effects include nausea, vomiting, and sedation. The most serious side effect is respiratory depression. Patients with any form of respiratory compromise must be kept under close observation following opioid administration; an oxygen saturation monitor may be useful. The opioid antagonist, naloxone, should be readily available. Opioid effects are dose-related, and there is great variability among patients in the doses that relieve pain and produce side effects.
Because of this, initiation of therapy requires titration to optimal dose and interval. The most important principle is to provide adequate pain relief. This requires determining whether the drug has adequately relieved the pain and the duration of the relief. The most common error made by physicians in managing severe pain with opioids is to prescribe an inadequate dose. Since many patients are reluctant to complain, this practice leads to needless suffering. In the absence of sedation at the expected time of peak effect, a physician should not hesitate to repeat the initial dose to achieve satisfactory pain relief. An innovative approach to the problem of achieving adequate pain relief is the use of patient-controlled analgesia (PCA). PCA requires a device that delivers a baseline continuous dose of an opioid drug, and preprogrammed additional doses whenever the patient pushes a button. The device can be programmed to limit the total hourly dose so that overdosing is impossible. The patient can then titrate the dose to the optimal level. This approach is used most extensively for the management of postoperative pain, but there is no reason why it should not be used for any hospitalized patient with persistent severe pain. PCA is also used for short-term home care of patients with intractable pain, such as is caused by metastatic cancer. Many physicians, nurses, and patients have a certain trepidation about using opioids that is based on an exaggerated fear of addiction. In fact, there is a vanishingly small chance of patients becoming addicted to narcotics as a result of their appropriate medical use.


The availability of new routes of administration has extended the usefulness of opioid analgesics. Most important is the availability of spinal administration. Opioids can be infused through a spinal catheter placed either intrathecally or epidurally. By applying opioids directly to the spinal cord, regional analgesia can be obtained using a relatively low total dose. In this way, such side effects as sedation, nausea, and respiratory depression can be minimized. This approach has been used extensively in obstetric procedures and for lower-body postoperative pain. Opioids can also be given intranasally (butorphanol), rectally, and transdermally (fentanyl), thus avoiding the discomfort of frequent injections in patients who cannot be given oral medication. The fentanyl transdermal patch has the advantage of providing fairly steady plasma levels, which maximizes patient comfort.

OPIOID AND CYCLOOXYGENASE INHIBITOR COMBINATIONS
When used in combination, opioids and COX inhibitors have additive effects. Because a lower dose of each can be used to achieve the same degree of pain relief and their side effects are nonadditive, such combinations can be used to lower the severity of dose-related side effects. Fixed-ratio combinations of an opioid with acetaminophen carry a special risk. Dose escalation as a result of increased severity of pain or decreased opioid effect as a result of tolerance may lead to levels of acetaminophen that are toxic to the liver.

CHRONIC PAIN
Managing patients with chronic pain is intellectually and emotionally challenging. The patient’s problem is often difficult to diagnose; such patients are demanding of the physician’s time and often appear emotionally distraught. The traditional medical approach of seeking an obscure organic pathology is usually unhelpful. On the other hand, psychological evaluation and behaviorally based treatment paradigms are frequently helpful, particularly in the setting of a multidisciplinary pain-management center.

There are several factors that can cause, perpetuate, or exacerbate chronic pain. First, of course, the patient may simply have a disease that is characteristically painful for which there is presently no cure. Arthritis, cancer, migraine headaches, fibromyalgia, and diabetic neuropathy are examples of this. Second, there may be secondary perpetuating factors that are initiated by disease and persist after that disease has resolved. Examples include damaged sensory nerves, sympathetic efferent activity, and painful reflex muscle contraction. Finally, a variety of psychological conditions can exacerbate or even cause pain.


There are certain areas to which special attention should be paid in the medical history. Because depression is the most common emotional disturbance in patients with chronic pain, patients should be questioned about their mood, appetite, sleep patterns, and daily activity. A simple standardized questionnaire, such as the Beck Depression Inventory, can be a useful screening device. It is important to remember that major depression is a common, treatable, and potentially fatal illness.


Other clues that a significant emotional disturbance is contributing to a patient’s chronic pain complaint include: pain that occurs in multiple unrelated sites; a pattern of recurrent, but separate, pain problems beginning in childhood or adolescence; pain beginning at a time of emotional trauma, such as the loss of a parent or spouse; a history of physical or sexual abuse; and past or present substance abuse. On examination, special attention should be paid to whether the patient guards the painful area and whether certain movements or postures are avoided because of pain. Discovering a mechanical component to the pain can be useful both diagnostically and therapeutically. Painful areas should be examined for deep tenderness, noting whether this is localized to muscle, ligamentous structures, or joints. Chronic myofascial pain is very common, and in these patients deep palpation may reveal highly localized trigger points that are firm bands or knots in muscle. Relief of the pain following injection of local anesthetic into these trigger points supports the diagnosis. A neuropathic component to the pain is indicated by evidence of nerve damage, such as sensory impairment, exquisitely sensitive skin, weakness and muscle atrophy, or loss of deep tendon reflexes. Evidence suggesting sympathetic nervous system involvement includes the presence of diffuse swelling, changes in skin color and temperature, and hypersensitive skin and joint tenderness compared with the normal side. Relief of the pain with a sympathetic block is diagnostic. A guiding principle in evaluating patients with chronic pain is to assess both emotional and organic factors before initiating therapy. Addressing these issues together, rather than waiting to address emotional issues after organic causes of pain have been ruled out, improves compliance in part because it assures patients that a psychological evaluation does not mean that the physician is questioning the validity of their complaint. Even when an organic cause for a patient’s pain can be found, it is still wise to look for other factors. For example, a cancer patient with painful bony metastases may have additional pain due to nerve damage and may also be depressed. Optimal therapy requires that each of these factors be looked for and treated.


TREATMENT of CHRONIC PAIN
Once the evaluation process has been completed and the likely causative and exacerbating factors identified, an explicit treatment plan should be developed. An important part of this process is to identify specific and realistic functional goals for therapy, such as getting a good night’s sleep, being able to go shopping, or returning to work. A multidisciplinary approach that utilizes medications, counseling, physical therapy, nerve blocks, and even surgery may be required to improve the patient’s quality of life. There are also some newer, relatively invasive procedures that can be helpful for some patients with intractable pain. These procedures include implanting intraspinal cannulae to deliver morphine or intraspinal electrodes for spinal stimulation. There are no set criteria for predicting which patients will respond to these procedures. They are generally reserved for patients who have not responded to conventional pharmacologic approaches. Referral to a multidisciplinary pain clinic for a full evaluation should precede any of these procedures. Such referrals are clearly not necessary for all chronic pain patients. For some, pharmacologic management alone can often provide adequate relief.


ANTIDEPRESSANT MEDICATIONS
The tricyclic antidepressants (TCAs) are extremely useful for the management of patients with chronic pain. Although developed for the treatment of depression, the tricyclics have a spectrum of dose-related biologic activities that include the production of analgesia in a variety of clinical conditions. Although the mechanism is unknown, the analgesic effect of TCAs has a more rapid onset and occurs at a lower dose than is typically required for the treatment of depression. Furthermore, patients with chronic pain who are not depressed obtain pain relief with antidepressants. There is evidence that tricyclic drugs potentiate opioid analgesia, so they are useful adjuncts for the treatment of severe persistent pain such as occurs with malignant tumors. TCAs are of particular value in the management of neuropathic pain such as occurs in diabetic neuropathy and postherpetic neuralgia, for which there are few other therapeutic options. The TCAs that have been shown to relieve pain have significant side effects . Some of these side effects, such as orthostatic hypotension, cardiac conduction delay, memory impairment, constipation, and urinary retention, are particularly problematic in elderly patients, and several are additive to the side effects of opioid analgesics.


The serotonin-selective reuptake inhibitors such as fluoxetine (Prozac) have fewer and less serious side effects than TCAs, but they are much less effective for relieving pain. It is of interest that venlafaxine (Effexor), a nontricyclic antidepressant that blocks both serotonin and norepinephrine reuptake, appears to retain most of the pain-relieving effect of TCAs with a side-effect profile more like that of the serotonin-selective reuptake inhibitors. The drug may be particularly useful in patients who cannot tolerate the side effects of tricyclics.

ANTICONVULSANTS AND ANTIARRHYTHMICS
These drugs are useful primarily for patients with neuropathic pain. Phenytoin (Dilantin) and carbamazepine (Tegretol) were first shown to relieve the pain of trigeminal neuralgia. This pain has a characteristic brief, shooting, electric shock–like quality. In fact, anticonvulsants seem to be helpful largely for pains that have such a lancinating quality. A newgeneration anticonvulsant, gabapentin (Neurontin), is effective for a broad range of neuropathic pains.


Antiarrhythmic drugs such as low-dose lidocaine and mexiletine (Mexitil) can also be effective for neuropathic pain. These drugs block the spontaneous activity of damaged primary afferent nociceptors.


CHRONIC OPIOID MEDICATION
The long-term use of opioids is accepted for patients with pain due to malignant disease. Although opioid use for chronic pain of nonmalignant origin is controversial, it is clear that for many such patients opioid analgesics are the best available option. This is understandable since opioids are the most potent and have the broadest range of efficacy of any analgesic medications.


Although addiction is rare in patients who first use opioids for pain relief, some degree of tolerance and physical dependence are likely with long-term use. Therefore, before embarking on opioid therapy, other options should be explored, and the limitations and risks of opioids should be explained to the patient. It is also important to point out that some opioid analgesic medications have mixed agonist-antagonist properties (e.g., pentazocine and butorphanol). From a practical standpoint, this means that they may worsen pain by inducing an abstinence syndrome in patients who are physically dependent on other opioid analgesics.


With long-term outpatient use of orally administered opioids, it is desirable to use long-acting compounds such as levorphanol, methadone, or sustained-release morphine. Transdermal fentanyl is another excellent option. The pharmacokinetic profile of these drug preparations enables prolonged pain relief, minimizes side effects such as sedation that are associated with high peak plasma levels, and reduces the likelihood of rebound pain associated with a rapid fall in plasma opioid concentration. Constipation is a virtually universal side effect of opioid use and should be treated expectantly. It is worth emphasizing that many patients, especially those with chronic pain, seek medical attention primarily because they are suffering and because only physicians can provide the medications required for their relief. A primary responsibility of all physicians is to minimize the physical and emotional discomfort of their patients. Familiarity with pain mechanisms and analgesic medications is an important step toward accomplishing this aim.

Related article : Understanding Pain

Understanding Pain

Because pain is universally understood as a signal of disease, it is the most common symptom that brings a patient to a physician's attention. Thus, understanding pain is very essential in order to preserve and restore health and to relieve suffering. The function of the pain sensory system is to protect the body and maintain homeostasis. It does this by detecting, localizing, and identifying tissue- damaging processes. Since different diseases produce characteristic patterns of tissue damage, the quality, time course, and location of a patient's pain complaint and the location of tenderness provide important diagnostic clues and are used to evaluate the response to treatment. Once this information is obtained, it is the obligation of the physician to provide rapid and effective pain relief.

THE PAIN SENSORY SYSTEM

Pain is an unpleasant sensation localized to a part of the body. It is often described in terms of a penetrating or tissue-destructive process (e.g., stabbing, burning, twisting, tearing, squeezing) and/or of a bodily or emotional reaction (e.g., terrifying, nauseating, sickening). Furthermore, any pain of moderate or higher intensity is accompanied by anxiety and the urge to escape or terminate the feeling.These properties illustrate the duality of pain: it is both sensation and emotion.

When acute, pain is characteristically associated with behavioral arousal and a stress response consisting of increased blood pressure, heart rate, pupil diameter, and plasma cortisol levels. In addition, local muscle contraction (e.g., limb flexion, abdominal wall rigidity) is often present.

Fig.1. Pprimary afferents with cell bodies in the dorsal root ganglion, and sympathetic postganglionic fibers with cell Components of a typical cutaneous nerve. There are two distinct functional categories of axons: bodies in the sympathetic ganglion. Primary afferents include those with large-diameter myelinated (Aβ), smalldiameter myelinated (Aδ), and unmyelinated (C) axons. All sympathetic postganglionic fibers are unmyelinated

PERIPHERAL MECHANISMS The Primary Afferent Nociceptor A peripheral nerve consists of the axons of three different types of neurons: primary sensory afferents, motor neurons, and sympathetic postganglionic neurons. The cell bodies of primary afferents are located in the dorsal root ganglia in the vertebral foramina. The primary afferent axon bifurcates to send one process into the spinal cord and the other to innervate tissues.

Primary afferents are classified by their diameter, degree of myelination, and conduction velocity. The largest-diameter fibers, A-beta (Aβ), respond maximally to light touch and/or moving stimuli; they are present primarily in nerves that innervate the skin. In normal individuals, the activity of these fibers does not produce pain. There are two other classes of primary afferents: the small-diameter myelinated

A-delta (Aδ) and the unmyelinated (C fiber) axons . These fibers are present in nerves to the skin and to deep somatic and visceral structures. Some tissues, such as the cornea, are innervated only by Aδ and C afferents. Most Aδ and C afferents respond maximally only to intense (painful) stimuli and produce the subjective experience of pain when they are electrically stimulated; this defines them as primary afferent nociceptors (pain receptors).

The ability to detect painful stimuli is completely abolished when Aδ and C axons are blocked. Individual primary afferent nociceptors can respond to several different types of noxious stimuli. For example, most nociceptors respond to heating, intense mechanical stimuli such as a pinch, and application of irritating chemicals.

Sensitization When intense, repeated, or prolonged stimuli are applied to damaged or inflamed tissues the threshold for activating primary afferent nociceptors is lowered and the frequency of firing is higher for all stimulus intensities. Inflammatory mediators such as bradykinin, some prostaglandins, and leukotrienes contribute to this process, which is called sensitization. In sensitized tissues normally innocuous stimuli can produce pain. Sensitization is a clinically important process that contributes to tenderness, soreness, and hyperalgesia. A striking example of sensitization is sunburned skin, in which severe pain can be produced by a gentle slap on the back or a warm shower. Sensitization is of particular importance for pain and tenderness in deep tissues. Viscera are normally relatively insensitive to noxious mechanical and thermal stimuli, although hollow viscera do generate significant discomfort when distended. In contrast, when affected by a disease process with an inflammatory component, deep structures such as joints or hollow viscera characteristically become exquisitely sensitive to mechanical stimulation.

Fig 2. Events leading to activation, sensitization, and spread of sensitization of primary afferent nociceptor terminals. A. Direct activation by intense pressure and consequent cell damage. Cell damage induces lower pH (H⁺)and leads to release of potassium (K⁺)and to synthesis of prostaglandins (PG) and bradykinin (BK). Prostaglandins increase the sensitivity of the terminal to bradykinin and other pain-producing substances. B. Secondary activation. Impulses generated in the stimulated terminal propagate not only to the spinal cord but also into other terminal branches where they induce the release of peptides, including substance P (SP).Substance P causes vasodilation and neurogenic edema with further accumulation of bradykinin. Substance P also causes the release of histamine (H) from mast cells and serotonin (5HT) from platelets.

A large proportion of Aδ and C afferents innervating viscera are completely insensitive in normal noninjured, noninflamed tissue. That is, they cannot be activated by known mechanical or thermal stimuli and are not spontaneously active. However, in the presence of inflammatory mediators, these afferents become sensitive to mechanical stimuli. Such afferents have been termed silent nociceptors, and their characteristic properties may explain how under pathologic conditions the relatively insensitive deep structures can become the source of severe and debilitating pain and tenderness. Low pH, prostaglandins, leukotrienes, and other inflammatory mediators such as bradykinin play a significant role in sensitization.

Nociceptor-Induced Inflammation One important concept to emerge in recent years is that afferent nociceptors also have a neuroeffector function. Most nociceptors contain polypeptide mediators that are released from their peripheral terminals when they are activated . An example is substance P, an 11-amino-acid peptide. Substance P is released from primary afferent nociceptors and has multiple biologic activities. It is a potent vasodilator, degranulates mast cells, is a chemoattractant for leukocytes, and increases the production and release of inflammatory mediators. Interestingly, depletion of substance P from joints reduces the severity of experimental arthritis. Primary afferent nociceptors are not simply passive messengers of threats to tissue injury but also play an active role in tissue protection through these neuroeffector functions.

CENTRAL MECHANISMS

The Spinal Cord and Referred Pain The axons of primary afferent nociceptors enter the spinal cord via the dorsal root. They terminate in the dorsal horn of the spinal gray matter . The terminals of primary afferent axons contact spinal neurons that transmit the pain signal to brain sites involved in pain perception. The axon of each primary afferent contacts many spinal neurons, and each spinal neuron receives convergent inputs from many primary afferents.

The convergence of sensory inputs to a single spinal pain-transmission neuron is of great importance because it underlies the phenomenon of referred pain. All spinal neurons that receive input from the viscera and deep musculoskeletal structures also receive input from the skin. The convergence patterns are determined by the spinal segment of the dorsal root ganglion that supplies the afferent innervation of a structure. For example, the afferents that supply the central diaphragm are derived from the third and fourth cervical dorsal root ganglia. Primary afferents with cell bodies in these same ganglia supply the skin of the shoulder and lower neck. Thus sensory inputs from both the shoulder skin and the central diaphragm converge on paintransmission neurons in the third and fourth cervical spinal segments.

Because of this convergence and the fact that the spinal neurons are most often activated by inputs from the skin, activity evoked in spinal neurons by input from deep structures is mislocalized by the patient to a place that is roughly coextensive with the region of skin innervated by the same spinal segment.

Thus inflammation near the central diaphragm is usually reported as discomfort near the shoulder. This spatial displacement of pain sensation from the site of the injury that produces it is known as referred pain.

Fig 3. The convergence-projection hypothesis of referred pain. According to this hypothesis, visceral afferent nociceptors converge on the same pain-projection neurons as the afferents from the somatic structures in which the pain is perceived. The brain has no way of knowing the actual source of input and mistakenly "projects" the sensation to the somatic structure.

Ascending Pathways for Pain A majority of spinal neurons contacted by primary afferent nociceptors send their axons to the contralateral thalamus. These axons form the contralateral spinothalamic tract, which lies in the anterolateral white matter of the spinal cord, the lateral edge of the medulla, and the lateral pons and midbrain. The spinothalamic pathway is crucial for pain sensation in humans. Interruption of this pathway produces permanent deficits in pain and temperature discrimination. Spinothalamic tract axons ascend to several regions of the thalamus.

There is tremendous divergence of the pain signal from these thalamic sites to broad areas of the cerebral cortex that subserve different aspects of the pain experience. One of the thalamic projections is to the somatosensory cortex. This projection mediates the purely sensory aspects of pain, i.e., its location, intensity, and quality.

Other thalamic neurons project to cortical regions that are linked to emotional responses, such as the cingulate gyrus and other areas of the frontal lobes. These pathways to the frontal cortex subserve the affective or unpleasant emotional dimension of pain. This affective dimension of pain produces suffering and exerts potent control of behavior. Because of this dimension, fear is a constant companion of pain.

PAIN MODULATION

The pain produced by similar injuries is remarkably variable in different situations and in different individuals. For example, athletes have been known to sustain serious fractures with only minor pain, and Beecher's classic World War II survey revealed that many soldiers in battle were unbothered by injuries that would have produced agonizing pain in civilian patients. Furthermore, even the suggestion of relief can have a significant analgesic effect (placebo).

Fig 4.

A. Transmission system for nociceptive messages. Noxious stimuli activate the sensitive peripheral ending of the primary afferent nociceptor by the process of transduction. The message is then transmitted over the peripheral nerve to the spinal cord, where it synapses with cells of origin of the major ascending pain pathway, the spinothalamic tract. The message is relayed in the thalamus to the anterior cingulate (C), frontal insular (F), and somatosensory cortex (SS).

B. Pain-modulation network. Inputs from frontal cortex and hypothalamus (Hyp.)activate cells in the midbrain that control spinal pain-transmission cells via cells in the medulla.

On the other hand, many patients find even minor injuries (such as venipuncture) frightening and unbearable, and the expectation of pain has been demonstrated to induce pain without a noxious stimulus. The powerful effect of expectation and other psychological variables on the perceived intensity of pain implies the existence of brain circuits that can modulate the activity of the pain-transmission pathways. One of these circuits has links in the hypothalamus, midbrain, and medulla, and it selectively controls spinal pain-transmission neurons through a descending pathway.

Human brain imaging studies have implicated this pain-modulating circuit in the pain-relieving effect of attention, suggestion, and opioid analgesic medications. Furthermore, each of the component structures of the pathway contains opioid receptors and is sensitive to the direct application of opioid drugs. In animals, lesions of the system reduce the analgesic effect of systemically administered opioids such as morphine.

Along with the opioid receptor, the component nuclei of this pain-modulating circuit contain endogenous opioid peptides such as the enkephalins and endorphin.

The most reliable way to activate this endogenous opioid-mediated modulating system is by prolonged pain and/or fear. There is evidence that pain-relieving endogenous opioids are released following surgical procedures and in patients given a placebo for pain relief.

Pain-modulating circuits can enhance as well as suppress pain. Both pain-inhibiting and pain-facilitating neurons in the medulla project to and control spinal pain-transmission neurons. Since pain-transmission neurons can be activated by modulatory neurons, it is theoretically possible to generate a pain signal with no peripheral noxious stimulus. In fact, functional imaging studies have demonstrated increased activity in this circuit during migraine headache. A central circuit that facilitates pain could account for the finding that pain can be induced by suggestion and could provide a framework for understanding how psychological factors can contribute to chronic pain.

NEUROPATHIC PAIN

Lesions of the peripheral or central nervous pathways for pain typically result in a loss or impairment of pain sensation.

Paradoxically, damage or dysfunction of these pathways can produce pain. For example, damage to peripheral nerves, as occurs in diabetic neuropathy, or to primary afferents, as in herpes zoster, can result in pain that is referred to the body region innervated by the damaged

nerves. Though rare, pain may also be produced by damage to the central nervous system, particularly the spinothalamic pathway or thalamus. Such neuropathic pains are often severe and are notoriously intractable to standard treatments for pain. Neuropathic pains typically have an unusual burning, tingling, or electric shock–like quality and may be triggered by very light touch.

These features are rare in other types of pain. On examination, a sensory deficit is characteristically present in the area of the patient's pain. Hyperpathia is also characteristic of neuropathic pain; patients often complain that the very lightest moving stimuli evoke exquisite pain (allodynia). In this regard it is of clinical interest that a topical preparation of 5% lidocaine in patch form is effective for patients with postherpetic neuralgia who have prominent allodynia.

A variety of mechanisms contribute to neuropathic pain. As with sensitized primary afferent nociceptors, damaged primary afferents, including nociceptors, become highly sensitive to mechanical stimulation and begin to generate impulses in the absence of stimulation. There is evidence that this increased sensitivity and spontaneous activity is due to an increased concentration of sodium channels.

Damaged primary afferents may also develop sensitivity to norepinephrine. Interestingly, spinal cord pain-transmission neurons cut off from their normal input may also become spontaneously active. Thus both central and peripheral nervous system hyperactivity contribute to neuropathic pain.

Sympathetically Maintained Pain Patients with peripheral nerve injury can develop a severe burning pain (causalgia) in the region innervated by the nerve. The pain typically begins after a delay of hours to days or even weeks. The pain is accompanied by swelling of the extremity, periarticular osteoporosis, and arthritic changes in the distal joints. The pain is dramatically and immediately relieved by blocking the sympathetic innervation of the affected extremity. Damaged primary afferent nociceptors acquire adrenergic sensitivity and can be activated by stimulation of the sympathetic outflow. A similar syndrome called reflex sympathetic dystrophy can be produced without obvious nerve damage by a variety of injuries, including fractures of bone, soft tissue trauma, myocardial infarction, and stroke .

Although the pathophysiology of this condition is poorly understood, the pain and the signs of inflammation are rapidly relieved by blocking the sympathetic nervous system. This implies that sympathetic activity can activate undamaged nociceptors when inflammation is present. Signs of sympathetic hyperactivity should be sought in patients with posttraumatic pain and inflammation and no other obvious explanation.