Gout can be extremely painful and incapacitating but is extremely treatable in almost all patients. It’s important to identify and treat it early to avoid pain and complications.
Author
Theodore Fields
Director, Rheumatology Faculty Practice Plan, Hospital for Special Surgery
New York, NY
1. Introduction:
Gout is an ancient disease associated with deposits of uric acid, especially in the joints and kidneys. It was described by Hippocrates, who noted its high male to female ratio and its association with alcohol. Dr. Thomas Sydenham (1624–1689) described the lumps of uric acid (called tophi) that can be seen in gout based on his own personal suffering. Until the early 19th century, however, gout was not well separated from other inflammatory types of arthritis. Only in the 20th century were the pathways of production of uric acid in the body clarified, and the ability of uric acid crystals to produce joint inflammation proven.
Gout can be extremely painful and incapacitating but is extremely treatable in almost all patients. Gout is most common in the big toe, and is also common in the mid-foot, ankle and knee. See #3 below for more details about how gout involves these and other joints. It’s important to identify and treat it early to avoid pain and complications. Women are not free of the risk of gout, and begin to “catch up” with men after they reach menopause. Although alcohol can bring on gout attacks, genetics are much more important than alcohol in defining who gets gout, and many who never drink alcohol suffer from gout. In fact, it is believed that the French royal families who suffered from gout developed this condition more because of lead poisoning from the casks used for their wine than from the wine itself, since lead injures the kidneys and impairs their ability to remove uric acid from the system. This situation has been mimicked in more recent times when imbibers of “moonshine whiskey,” often made in radiators containing lead, developed a lead poisoning-associated gout (“Saturnine gout”). Excess body weight has also been associated with gout. The prosperous and overweight burgher with gout is a classical image of the 1800’s, but gout in reality affects those in all financial circumstances.
Gout is a common disease. It has been estimated that there may be as many as 5 million gout sufferers in the United States. Even more conservative estimates put this number at greater than 2 million (Mayo Clinic estimate). Population studies from both the Mayo Clinic and from Taiwan have shown significant increases in the prevalence of gout recently as compared to 20 years ago. The prevalence of gout has increased in both older and younger people. The increase in younger people is not explained, but the increase in older people, at least in part, relates to increased life span, increased weight (obesity is associated with gout) and increased use of diuretics. Diuretics are used commonly for hypertension, for example, and they elevate the blood levels of uric acid and can increase the risk of gout.
Gout is best understood by seeing it as having four stages (Figure 1- stages of gout). The first phase is elevated uric acid without gout or kidney stone, a phase which has no symptoms and is generally not treated. The second phase is the “acute attack” – with pain and inflammation. The third phase is the “time between attacks” when a person feels normal but is at risk for recurrence. The final phase is “chronic gouty arthritis,” where there are “lumps” of uric acid, or tophi (Figure 2 a and 2b– illustration of normal toe joint and of gouty tophus), frequent attacks of acute gout, and often a degree of pain even between attacks (Figure 3- progression of gout).
2. Who gets gout and why?
Gout is clearly associated with a buildup of uric acid. Uric acid is a produced as part of the body’s metabolism of purines, which are produced as the body breaks down any of the many purine-containing substances, including nucleic acids from our diet or from the breakdown of our own cells. Figure 4, on the left side, shows a simplified pathway from purines to uric acid, and on the right shows how medications for gout work, which is discussed further in sections 5 and 6 below (Figure 4- pathway from purines to uric acid). Depending on the lab, normal values for uric acid run from 3.6 mg/dL to 8.3 mg/dL. The higher the blood level uric acid, the more the risk of deposits of uric acid in the joints and subsequent gouty attacks. In mammals other than man and the great apes, the enzyme uricase breaks uric acid into the more soluble allantoin, which can be more easily excreted in the urine. Humans, lacking this enzyme, run higher levels of uric acid and are thus subject to gout.
Gout can develop in a person either because they are producing too much uric acid or because they are unable to put enough of it into the urine (or both). The most common cause of gout (about 90% of cases) is the inability to excrete enough uric acid in the urine. This inability may occur for a number of reasons. The most common is a genetic defect in substances referred to as organic anion transporters in the kidney, which leads to an excessive reabsorption of uric acid from the kidney—and thus too much uric acid in the blood. However, a defect in excretion of uric acid can also occur due to medications, such as diuretics, low dose aspirin, or alcohol. Defective uric acid excretion also occurs when the kidneys are functioning poorly.
About 10% of cases of gout are due to overproduction of uric acid. When uric acid is overproduced, it is high not only in the blood but in the urine, raising the risk of both gout and kidney stone. Some people overproduce uric acid due to a genetic defect in an enzyme in the purine breakdown pathway (see figure 4) which leads to overactivity of this pathway. Since cells contain DNA, and DNA contains purines, anything that increases the breakdown of cells in the body can lead to more uric acid and gout. For example, if a patient is receiving chemotherapy for a tumor, as the treatment kills the tumor cells a gout attack or kidney stone can develop as a result of the breakdown of the purines from those cells. Foods can also lead to overproduction of uric acid, such as meats and meat gravies and beer, which contain high levels of purines.
Men get gout more than women, and at younger ages, the male to female ratio is 9:1. The most common age of onset is from age 40- 60 years. Gout is fairly rare in women until they reach menopause. One theory is that estrogen blocks the anion exchange transporter (see above) in the kidney, causing more uric acid to be excreted in the urine, and thus lower the level of uric acid in the blood. Gout most commonly starts in a person’s 40’s to 60’s, although it can start earlier than the 40’s for those with a genetic predisposition, and it can also occur for the first time when someone is in their 80’s. In some cases, injuries can set off an attack of gout. A “stub of the toe” can lead to a gout attack if there were already enough uric acid crystals saturating the cartilage.
Whatever the mechanism of the elevated uric acid, the key event in gout is the movement of uric acid crystals into the joint fluid. The body’s defense mechanisms, including the white blood cells (neutrophils) engulf the uric acid crystals, which leads to a release of inflammatory chemicals (called cytokines) which cause all the signs of inflammation, including heat, redness, and swelling and pain. This cycle also recruits more white blood cells to the joint which accelerates the inflammatory process.
When thinking of gout, a useful model has been proposed by Wortmann.1 Uric acid crystals can be thought of like matches, which can sit quietly or can be ignited. Crystals can be present for years in the cartilage, or even in the joint fluid, without causing inflammation. Then, at some point, due to increasing number of crystals or other inciting factor, the matches are “struck” and the inflammation begins. This analogy is important both for conceptualizing the uric acid crystals in the joint and for understanding the various types of gout treatment (see below) – some of which attack the inflammation (pour water on the flaming matches) and some of which remove the uric acid crystals (take away the matches).
3. What joints are involved in gouty arthritis, and what does a gout attack look and feel like?
As with all other known types of arthritis, gout has particular joints it tends to attack. Gout especially favors the bunion joint, known as the 1st metatarso-phalangeal joint, which is the first joint involved in 75% of patients and is ultimately involved in over 90% of those with this condition. (Figure 5- Location of Gout Attacks). The ankle, mid-foot and knee are also common locations for gout, as well as the bursa that overlies the elbow. Late in gout, if untreated, multiple joints can be involved, including the fingers and wrists. The shoulder joint is very rarely involved by gout, and the hip essentially never.
When gout occurs, the joint tends to be extremely painful and is warm, red and swollen (Figure 6- Toe with Acute Attack of Gout). The inflammation that is part of a gout attack is systemic, so that fever and chills, fatigue and malaise are not uncommonly part of the picture of a gout attack.
Gout attacks can occur in joints that look normal, or in joints that have easily visible deposits of uric acid. These deposits are called tophi (See figures: 7 A and 7B: tophi on foot and over Achilles' tendon, figure 8: tophus on elbow, figure 9: tophi on hands, and figure 10: large tophus of finger). and can be in numerous locations, but especially on the feet and elbows. In figure 9, the little finger of the right hand is bandaged since fluid was just removed from it, which demonstrated innumerable uric acid crystals.
While some gout attacks will resolve quickly by themselves, the majority will go on for a week, several weeks or even longer if not treated. Since gout attacks are usually quite painful, and often make walking difficult, most gout sufferers will request specific treatment for their painful condition.
4. How is gout diagnosed?
Since the treatment for gout is lifelong, it’s very important to make a definitive diagnosis. In a clear-cut case, a primary care physician can make the diagnosis of gout with a high level of confidence, but often there are two or more possible causes for an inflamed toe or other joint which has some of the features of gout. Ideally, the diagnosis is made by identifying uric acid crystals in joint fluid or in a mass of uric acid (tophus). These can be seen by putting a drop of fluid on a slide and examining it using a polarizing microscope, which takes advantage of the way uric acid crystals bend light. A non-rheumatologist, when possible, can remove fluid from the joint, by aspirating it with a small needle, and send it to a lab for analysis. A rheumatologist is likely to have a polarizing attachment on their microscope at their office. Gout crystals have a needle-like shape, and are either yellow or blue depending on how they are arranged on the slide (see figure 11: Uric Acid Crystals Under Polarizing Light Microscopy).
There are many circumstances where, however ideal it would be, no fluid or other specimen is available to examine, but a diagnosis of gout needs to be made. A set of criteria has been established to help make the diagnosis of gout in this setting (See Table 1- Diagnosis of Gout When No Crystal Identification Possible).2 These criteria take advantage of the features of gout that separate it from other types of inflammatory arthritis, such as rheumatoid arthritis. For example, the inflammation of gout tends to reach a maximum within 24 hours, while other types of arthritis tend to evolve more slowly. Likewise, the presence of redness over a joint, the involvement of the “bunion” joint and a high blood level of uric acid are all features making gout more likely. The diagnosis of gout is made in the presence of 6 of the 10 criteria listed in Table 1.
_____________
Table 1: Diagnosing Gout When No Crystal Identification is Possible
Ideally 6 of 10 features will be present of the following:
1. Inflammation reaches a maximum within one day (rapid acceleration of inflammation).
2. Having a history of similar episode of inflammation
3. Attack of arthritis in a single joint.
4. Redness over an involved joint (gout is highly inflammatory)
5. Involvement of the base of the big toe on one side (the most common site for gout)
6. Involvement of the joints at the middle of the foot
7. Uric acid elevation on blood testing
8. X-ray findings of swelling of joints which is not symmetrical
9. Joint fluid is tested for infection and is negative.
10. X-ray shows characteristic changes of gout, including cysts in bone and erosions.
_____________
When the diagnosis of gout is made, the individual must be evaluated for the complications of gout. Collections of uric acid, tophi, need to be searched for, and they can be in numerous locations (see figures 7-10). Inquiry should be made regarding a history of kidney stone, since a patient with gout and kidney stones will likely require faster and more aggressive lowering of uric acid (see below) than one without stones, to try and prevent recurrent stone formation. A patient with gout has been shown in a broad range of studies to be at higher risk of coronary disease, and should have an evaluation appropriate to coronary risk (e.g. lab testing for cholesterol and triglyceride level).3
X-rays and other studies, such as Magnetic Resonance Imaging (MRI) and ultrasound of the affected joints, can demonstrate the changes of gout. It is important that damage to bone from gout be diagnosed, since documented damage is a clear indication for long-term therapy (see below). Once damage has begun, it’s important to reduce the total body uric acid level and which the, by equilibration, causes uric acid to move out of the joints. This is because the blood and joint levels of uric acid reach a certain level, called a “steady state,” at a given level of blood uric acid. If the blood level is reduced, then the joint level of uric acid will gradually decrease as well. This leads to gout attacks diminishing or completely ceasing over time, and to tophi getting reabsorbed and shrinking or fully disappearing. Different approaches can be taken to lowering total body uric acid. The production of uric acid can be decreased in the body (e.g. by allopurinol- see below) or the excretion of uric acid can be increased (e.g. by probenecid, see below). The crystals can also be broken down in the body (see 7a below re Rasburicase and 7b below be pegylated uricase), but using this mechanism is still under study at this time. This can help prevent further damage. X-rays are the standard imaging technique for gout (See figures 12 through 17: figure 12: gout of the base of the 1st toe; figure 13: gout of the distal finger joints; figure 14: gouty change and soft tissue calcification about the base of the 1st toe; figure 15: gouty destruction at multiple finger joints; figure 16: gouty erosion at the proximal ulna at the elbow; figure 17: large tophus seen as soft tissue mass at the elbow) but in special cases, such as when gout needs to be separated from infection or tumor, MRI (figure 18: MRI of the knee showing gouty soft tissue mass and erosion of the kneecap) or ultrasound (figure 19: Power Doppler study showing gouty inflammation at the base of the 1st toe) will be helpful.
The red and hot joints, coupled with rapid acceleration of joint pain, strongly suggest gout, and identifying tophi, if present (see figures 7-10) help further. Special effort should be made to distinguish gout from the other crystal-induced types of arthritis. For example, pseudogout, caused by a different type of crystal (calcium pyrophosphate), causes the same type of hot, red joint, and the same rapid acceleration of pain as does gout. Pseudogout can be distinguished by seeing calcium deposits within the joints on x-ray, which deposits in a different way than it does in gout. When fluid is examined from an inflamed joint in pseudogout, the specific causative crystal can be seen. A third type of crystal-induced arthritis, hydroxyapatite deposition disease, has a type of crystal that needs special studies (one such study is electron microscopy) for identification. The presence of these other types of crystal-related inflammation further emphasizes the value of identifying uric acid crystals as the cause of a particular patient’s arthritis whenever possible, to insure that the correct condition is being treated.
5. How can an attack of gout be treated?
The management of an acute attack of gout is very different from the prevention of subsequent attacks. See figure 4 for overall approach to treatment and prevention of gout. Treatments used for prevention, such as allopurinol (see below) can actually make things worse if given during an attack, and so need to be held back until the attack has resolved for several weeks. There are a number of measures that can help resolve an attack of gout. See Table 2 for summary of treatment strategies for acute gout. One principle is that treatment for an attack of gout should be instituted quickly, since quick treatment can often be rewarded with a quick improvement. If an attack of gout is allowed to last more than a day or so before treatment is started, the response to treatment may be much slower.
____________
Table 2: Medications to Treat Acute Attacks of Gout
1. Non-steroidal anti-inflammatory drugs (NSAID's) or COX-2 inhibitors. Examples of NSAID's: Naproxen 500mg twice daily, indomethacin 25mg three times daily. Example of COX-2 inhibitor: celecoxib 200mg twice a day. Possible side-effects: Elevation of blood pressure, ankle swelling, upset stomach, ulcer (long-term use may have an increased risk of heart attack or stroke, but gout use is generally very short-term). Use with caution if kidney or liver problems.
2. Anti-Inflammatory corticosteroids. Examples: Prednisone 40mg first day, 30mg 2nd day, 20mg third day, 10mg fourth day. Possible side-effects: Elevation of blood pressure, elevation of blood sugar, mood changes. Short-term use, as in gout, generally much better tolerated than long-term use. Use with caution if diabetic.
3. Colchicine. In the past, high doses of colchicine were used for gout attacks, but this tended to cause diarrhea in a large number of patients. It has been shown that lower doses of colchicine are as effective as high doses for an attack of gout, and much better tolerated. Assuming no other medical problems that require an adjusted dose, for an attack of gout a patient would receive 2 tablets of colchicine, 0.6mg each, as soon as possible after a gout attack starts. They would then receive one additional tablet an hour later. Colchicine dose needs to be adjusted in patients with significantly decreased kidney function. Colchicine has interactions with certain other medications, most notably clarithromycin (Biaxin®).
4. Local steroid injections. Example: different doses used depending on the size of joint involved, and multiple preparations available. Possible side-effects: 1-2% of the time, a local reaction to the injection can occur, and the joint can can temporary worsening the next day, requiring ice application. In diabetics, a single local injection can temporarily raise blood sugar.
____________
a) Physical measures in treating an acute attack of gout: It is important to get off the foot if the gout attack is in the lower extremity. Trying to ignore the attack can lead to a more prolonged duration. Local ice has been shown to help (for not more than 10 minutes at a time, to avoid skin damage). Leg elevation is helpful for some.
b) Medications for acute gout:
1. Non-steroidal anti-inflammatory agents and COX-2 inhibitors are the mainstay of therapy of acute attacks of gout in patients who have no contra-indication to them. These medications include such agents as naproxen (Naprosyn®), ibuprofen (Motrin®), celecoxib (Celebrex®), indomethacin (Indocin®) and many others. These agents reliably decrease the inflammation and pain of gout. However, patients with ulcers, hypertension, coronary disease and fluid retention must be careful with these agents, even for the short courses (usually 3-7 days) needed to resolve a gout attack. The doses of non-steroidal anti-inflammatory agents needed to resolve a gout attack are on the higher side, since full anti-inflammatory effect is needed. See examples of dosage in Table 2. Over-the-counter dosage levels, e.g. ibuprofen at 200mg, 2 tabs three times a day, are often insufficient.
2. Corticosteroids, such as prednisone and methylprednisolone (Medrol®), are anti-inflammatory agents that are quite effective against gout attacks. Anti-inflammatory steroids are very different in action and side-effects as compared to male hormone steroids. Anti-inflammatory steroids have long-term risks, such as bone thinning and infection, but their risk for short-term (e.g. 3-7 days) therapy is relatively low. These agents can raise blood pressure and blood sugar, so can be a problem for those with uncontrolled hypertension or uncontrolled diabetes mellitus.
3. Colchicine (Colcrys®) has a role in both the prevention and treatment of gout attcks (see below for discussion of its role in prevention). See details about colchicine for attacks of gout in Table 2. An attractive feature of colchicine is how specific it is. For example, it can resolve an attack of gout, but it doesn't help a flare-up of rheumatoid arthritis. If the level of colchicine builds up too high, as it might if a usual dose is given to a patient with severe kidney disease, toxicity can occur, such as suppression of the production of blood cells. In the past, colchicine was also used intravenously in addition to its oral use. Intravenous use can be very effective, and doesn't cause diarrhea by this route, but this agent must be given extremely carefully, since an error in dosing can shut down the bone marrow’s production of blood cells, and potentially be fatal. For this reason, intravenous colchicine is very rarely used today. Patients often ask about why colchicine, which has been available in unbranded form for many years, is now a branded drug (Colcrys®). This is a result of the FDA effort to review and standardize the production of drugs which have been around a long time and were not previously reviewed by FDA. Colchicine is one of a small number of drugs where new studies were done (e.g. of drug interactions and re-evaluation of dosing) where the FDA has granted brand status to a manufacturer despite the unbranded form having long been available.
4. Local injection of crystalline preparations of corticosteroid can be an excellent option if a person has a single joint gout attack. Formulations injected include methylprednisolone acetate (Depo-Medrol®), triamcinolone (Aristospan®), and betamethasone (Celestone®). Of these preparations, betamethasone lasts the shortest time in the joint of these preparations, but gout tends to be self-limited within a few weeks in any case so this option can be quite successful. The advantage of betamethasone is a decreased likelihood of temporarily worsened flares the day after the injection, which is the most common adverse reaction to local steroid injections. Local injection also carries a very small risk of introducing an infection into the joint, but has the advantage that if gout has not as yet been definitively diagnosed, a sample of fluid can be obtained via the same needle and analyzed for the presence of uric acid crystals.
6. How can an attack of gout be prevented?
a) The role of diet in gout prevention: Since foods can directly set off gout attacks, it is clear that patients with gout should receive counseling as to which are more likely to induce attacks. Dietary control may be sufficient in a patient with mildly elevated uric acid, e.g. 7.0 mg/dL (noting that any uric acid level above 6.0 is considered elevated for a patient with gout, even if within what the lab calls the “normal range.)” For those with a higher level, e.g. 10.0 mg/dL, diet alone will not usually prevent gout. For the latter, even a very strict diet only reduces the blood uric acid by about 1 mg/dL- not enough, in general, to keep uric acid from precipitating in the joints. The cutoff where patients with gout seem to dramatically reduce their number of attacks is when their uric acid level is taken below 6.0 mg/dL.4
With the above qualifications, attention to diet in gout patients is helpful, and especially so when first starting medication to lower the uric acid (which may, paradoxically, initially set off gout attacks). There are a few basic principles of diet in gout which have stood up to a variety of studies: limit red meat and meat gravies, limit shellfish, and limit alcohol, especially beer.5,6 Red meat and shellfish (e.g. scallops, shrimp and mussels) should, ideally, be eaten less frequently, in smaller portions (e.g. 3 oz). All types of alcohol cause more uric acid to be reabsorbed by the kidneys, raising blood uric acid levels, but beer has its own high purine level and so contributes to blood uric acid elevation in two different ways. Vegetable protein is broken down to purine, but does not seem to be a significant contributing factor in gout. Low fat dairy products, despite mild protein being broken down to purine, likewise seems not to contribute to gout risk (and may even be protective).5 Certain carbohydrates, such as oatmeal, wheat germ, and bran have moderate purine content but have not been shown to be significant gout risk factors. For those interested in achieving the maximal lowering of uric acid by dietary means, two “Gout Haters Cookbooks” are listed in “Books about Gout” below and all four of these cookbooks can be found at http://www.gout-haters.com.
b). The role of physical activity in prevention of gout: Along with diet, physical activity can help with weight loss, and gout has been associated with being overweight.7 in patients with well-established gout, especially if x-rays have demonstrated joint damage in the foot, a low-impact exercise program is reasonable. An exercise program combined with diet in gout can reduce risk for attacks.7 If an attack seems to be coming on in the lower extremity, patients are well-advised to try to get off their feet, since impact seems to worsen gout attacks. Clues to an attack of gout coming on include local swelling, heat, redness and tenderness in a joint, especially in the foot, ankle or knee. Some patients have fever and chills as the first warning that an attack of gout is coming on.
c) The role of medication in prevention of gout (see Table 3 for summary of medications to prevent gout attacks):
_________________________________________________________________________________________
Table 3: Medications to Prevent Attacks of Gout
1. Allopurinol: to decrease production of uric acid
2. Probenecid: to increase the excretion of uric acid
3. Colchicine: to decrease the ability of uric acid crystals to cause inflammation.
________________________________________________________________________________________
1. Standard medications in preventing gout attacks:
i. Colchicine (Colcrys®): using the “matches” analogy discussed above1, using colchicine can be seen as “dampening” the uric acid “matches.” Colchicine does not lower the body’s store of uric acid, but it decreases the intensity of the body’s inflammatory reaction to these crystals. Recent studies have shown that at least one mechanism of colchicine’s action is by acting to prevent a cascade of reactions that lead to the production of interleukin 1-beta, which is an inflammatory protein (cytokine), which is important in gouty inflammation.8 When used as one or two tablets a day (0.6mg each), most people tolerate this medication well, and this dose can help prevent gout attacks. Some physicians would start colchicine after one very severe or two moderately severe attacks of gout, and beyond that use allopurinol. If a patient has two attacks of gout within the same 12 months, it is generally recommended that they be treated with a medication to lower the uric acid, which colchicine does not accomplish. See below for discussion of the uric acid-lowering agents, allopurinol and probenecid. There is a rare effect on the nerves and muscles with long-term use of colchicine, and a blood test from the muscle (CPK) is monitored at approximately 6 month intervals in patients taking colchicine on a regular basis. Colchicine also has a major role when patients are beginning therapy with allopurinol (see below) to prevent the increase in gout attacks that can happen when allopurinol is begun. The colchicine, in that case, is often withdrawn at about 6 months, assuming no gout attacks have occurred.
ii. Allopurinol: This agent is presently the most commonly used drug for the prevention of gout. Allopurinol blocks the enzyme xanthine oxidase, which blocks the breakdown of purines, thus decreasing the body’s total amount of uric acid. Allopurinol is effective in preventing gout no matter what the mechanism of the elevated uric acid was. Whether a person is making too much uric acid, or has difficulty excreting it via the kidney, allopurinol’s decrease in uric acid production leads to the same goal: a decreased total body uric acid. Within a week after taking a dose, uric acid is significantly lowered by allopurinol. The most common adverse reaction to allopurinol is an increase in gout attacks early in therapy. For this reason it is initially often started together with colchicine (see above), so that while the “matches”1 are slowly removed, those remaining are “dampened.” Other adverse reactions to allopurinol include skin rash, abnormality of liver blood tests, and occasionally drop in the white blood cell count. Ampicillin, an antibiotic, seems to cause more rashes in patients already taking allopurinol. A rare but very serious side-effect is the allopurinol hypersensitivity syndrome, which can present with severe rash along with severe liver and blood cell abnormality. This syndrome has been reported to be more likely if the patient has abnormal kidney function.9 Although there is some significant debate on this point10, it is generally agreed that patients with abnormal kidney function should start allopurinol at low doses and build up, to ensure that the allopurinol is effectively excreted. The level of uric acid in these patients is followed closely, and the level of uric acid is used as a guide as the allopurinol dose is slowly increased. The severity of the allopurinol hypersensitivity syndrome is a reminder that specific criteria must be used to decide which patients should be treated with allopurinol (See Table 4: Reasons to Use Medication to Lower Uric Acid).
_____________________________________________________________________________________________
Table 4: Reasons to Use Medication to Lower Uric Acid
1. Gout with more than two attacks a year, whether due to overproduction of uric acid or difficulty excreting it.
2. Chronic visible collections of uric acid (tophi)
3. High uric acid in the urine (over 800mg per 24 hours), especially if history of kidney stone
4. Failure of other options to control the arthritis of gout (e.g. failure of probenecid)
5. When a person is receiving chemotherapy for a leukemia or a lymphoma and it is expected that many tumor cells will be killed (since one of the breakdown products of cells is purine which gets broken down to uric acid).
____________________________________________________________________________________________
iii. Febuxostat (Uloric®): this medication was approved by the FDA in February 2009 for treating patients with gout by lowering their uric acid levels. It works similarly to allopurinol in that it inhibits xanthine oxidase, a key enzyme in the pathway that produces uric acid, and thereby reduces total body uric acid level. Like allopurinol, the most common side-effect of febuxostat is causing gout to flare after this drug is started. As with allopurinol, it is reasonable whenever possible to add a preventative medication, such as colchicine, for at least the first 6 months after starting febuxostat to help avoid gout flares. Later on, as the total body uric acid decreases, this will generally no longer be needed. One potential advantage of febuxostat is that it is structurally quite different from allopurinol, and therefore likely can be used in patients who are allergic to allopurinol. Only a limited number of patients who were allergic to allopurinol have been studied to date, but the drug was tolerated in those patients. Another advantage is that its excretion is handled more by the liver than the kidney, unlike allopurinol, and febuxostat may thus have some advantage in patients with kidney dysfunction. Unlike allopurinol, which interacts with warfarin (Coumadin®), febuxostat did not have this interaction when studied. Febuxostat is approved by the FDA to start at 40mg daily, and if the uric acid has not reached goal (less than 6.0mg/dL) after two weeks of treatment the dose can be increased to 80mg daily. The 80mg dose of febuxostat brought more patients to less than 6mg/dL of uric acid than 300mg of allopurinol, the dose of allopurinol most commonly used. Rheumatologists often adust allopurinol doses higher than 300mg when needed to reach uric acid goal, although the literature on higher doses of allopurinol is limited. Patients with controlled uric acid level and doing well on allopurinol would seem to have no reason to switch to this new agent, in view of allopurinol's lower cost and 40 year history of an overall very good safety record (see "Allopurinol" discussion above).
iv. Probenecid: This medication increases the amount of uric acid that is excreted in the urine, by decreasing the amount that gets reabsorbed by the kidney. Medications that can cause more uric acid to come out in the urine are called uricosuric agents. Probenecid is the main such agent used in the U.S. Probenecid can be successful in bringing the blood uric acid below 6.0, and reducing or preventing gout attacks. Like allopurinol, an increased number of gout attacks can occur when probenecid is started, and for this reason colchicine is often given for the first 6 months of therapy. Unlike allopurinol, however, early in therapy probenecid can increase urinary uric acid, which could lead to the development of a kidney stone. For this reason, it is reasonable to check a 24 hour urine for uric acid before probenecid is started, and if this result is >800mg/24 hour this therapy should be reconsidered. If the result is borderline, at a minimum the patient is advised to drink extra fluids, to help prevent kidney stones early on in treatment. There are also medications that can change the acidity of the urine, and by alkalinizing the urine in such a case the risk of kidney stone can be decreased (uric acid is more soluble in alkaline medium, so less likely to crystallize). Probenecid can also cause a rash, but seems less likely than allopurinol to cause a very severe hypersensitivity reaction. Probenecid is not effective if a patient has kidney dysfunction [creatinine greater than 2.0 – (creatinine is a measure of a waste product excreted by the kidney]). Because of the above limitations, allopurinol is often used as the drug of choice in a patient where lowering uric acid is the goal, but there remains a place for probenecid in the armamentarium against gout.
v. Pegylated uricase- pegloticase (Krystexxa®): This intravenous medication is extremely potent at markedly lowering the uric acid level quickly. It was approved in late 2010 for use in gout patients who have failed or were intolerant to both allopurinol and febuxostat. It appears that tophi shrink more quickly with this agent than with any other agent used to treat gout. An earlier Phase II trial13 and two essentially identical Phase III trials(a study of at least moderate size that compares a new treatment with the current standard of care in patients), Gout 1 and Gout 2 have been presented.14 Data on shrinkage of tophi with this agent was also presented in 6/09.15 Cardiac events have occurred during the studies of Krystexxa®, and the FDA reviewed them closely and concluded that they did not appear due to the medication. There were also allergic-type events and events where pateints dropped their blood pressure while this intravenous agent was running into them. None of these episodes of drop in blood pressure led to death or long-term problems problems for the patients, however, and the blood pressure returned to baseline in these cases. The drop in blood pressure is still a concern, and this medication must be used in a setting where treatment of the drop in blood pressure can be managed. Pegloticase may be especially useful in patients with very large collections of uric acid (tophi), especially if these are draining to the skin. Like Uloric®, Krystexxa® does not appear dependent on the kidney to be removed from the body, allowing it to be considered in patients with decreased kidney function. Because Krystexxa® is given intravenously, it would be expected that the great majority of its use would be by rheumatologists rather than by internists or primary care physicians.
2. What if a patient can't take the usual medications? If a patient is allergic to allopurinol, there are often limited options. If the rash was relatively mild, one option is an oral desensitization regimen for that agent.11 This involves having a pharmacist put together a solution of allopurinol of very low and then gradually increasing concentrations over the course of a month. Although at times the rash will reoccur during this process, often a patient can be desensitized in this way and subsequently tolerate allopurinol. Although some patients develop a mild rash to allopurinol that remains mild over time, or respond to antihistamines, continuing the allopurinol despite a rash is not advised, since the rash can worsen unpredictably.
If a patient can’t tolerate allopurinol, and meets the criteria (see above) for probenecid, that can be tried. There are some medications which are used for other indications but that have modest effect in lowering uric acid levels, such as losartan (Cozaar®), used for hypertension , and fenofibrate (Tricor®), used for elevated triglycerides, but these only infrequently can sufficiently lower uric acid level.
If none of the above options is possible or successful, physicians often seek a clinical trial of a new agent for gout, if available, for their patient to enter. See section 7 below for a discussion of agents presently under study for gout. Online resources, such as http://clinicaltrials.gov, can help to identify clinical trials.
3. Alternative/complementary medications/supplements: Gout is a common disease and many medications and supplements have been tried. Cherry juice has long been an alternative remedy which had anecdotal support now has been studied. At the American College of Rheumatology meeting in November 2010 (data available at www.rheumatology.org) there were two studies looking at cherry juice. It appears that cherry juice may have a small effect in decreasing production of uric acid. It also, possibly through its vitamin C content, can increase the excreton of uric acid by the kidney. In separate earlier study, vitamin C itself did appear to increase uric acid excretion. However, the effect (using 500mg a day dosing) was small-- only a drop in blood uric acid level of about 0.5 mg/dL, and almost all gout patients need to come down more than this to get to the goal of less than 6.0 mg/dL. These early studies of cherry juice are interesting, and might be relevant for a patient who was "almost there" in their uric acid goal, but a gout sufferer should be very careful about trusting to cherry juice to manage their uric acid. Based on the data, the result is likely not going to be sufficient.
Diet has been discussed in more detail above, and gout is clearly one of the rheumatic diseases where diet is unequivocally important. Devil’s claw (Harpagophytum procumbens) and many other herbal treatments have been proposed as gout therapy, and further study of these is indicated. The main message of this review is to emphasize how dramatically effective standard medication is for gout, both in acute treatment and prevention. The safety profile of treatments for gout is generally quite good, despite the caveats mentioned above, e.g. in the discussions of “colchicine” and “allopurinol.” For this reason, I believe that the great majority of gout sufferers would be well-served to explore traditional options for gout first and then choose their options. Many of my patients have explored a variety of non-traditional approaches to gout, often in combination with traditional measures. My personal feeling is that herbal and other alternative/complementary approaches may well ultimately be proven to improve inflammation in gout, but lowering uric acid is the key to success in gout management. Our present agents, such as allopurinol and probenecid, are so effective, and reasonably safe and predictable, that it seems unlikely that they will be fully displaced in the future. However, there are a small but very important group of patients who cannot tolerate these present agents. The development of new uric acid-lowering treatments, with even fewer side-effects than our present agents, would be heartily welcomed.
7. What are future possible treatments of gout?
Fortunately, present medications are successful in the vast majority of gout patients. Some patient cannot tolerate our present arsenal of gout medications, and for some these agents are not sufficiently effective. Therefore, new treatments are continually being sought. Some of the more promising ones follow:
a) Anakinra (Kineret®): this biologic agent is presently approved by the FDA for the treatment of rheumatoid arthritis. It works to block the receptor for interleukin 1-beta, an important inflammatory chemical (cytokine). Since interleukin 1-beta has been shown to be a key player in gouty inflammation (see under “colchicine for acute gout” above), this agent has been studied in the treatment of gout attacks, and appears to have been successful in preliminary study.16
b) Rilonacept (Arcalyst®) is a fusion protein which acts as a blocker of interleukin 1- beta, and it has a longer duration of action than anakinra. This agent has been studied in a 14 week trial and showed improvement in gouty symptoms.17 This agent may have a future role in preventing gout attacks when patients are started on a uric acid lowering agent but can take the usual prophylactic agents against the attacks that often are an early result of this therapy (e.g. they can't use colchicine). There may also be selected patients where rilonacept treatment might be a longer-term alternative.
c) Canakinumab (Ilaris®) is a human monoclonal antibody which targets interleukin 1- beta, and a recent abstract looked at its ability to treat and prevent gout attacks, and showed some success.18 As with rilonacept above, this agent may have a future role in the acute treatment and relatively short-term prevention of gout, and may have a longer-term role in selected patients with problems with multiple other options.
d) Urate reasbsorbtion blocker (presently called RDEA594): this agent is a direct blocker of URAT1, which is the transporter of uric acid from the urine back into the body. This blockage leads to more excretion of uric acid in the urine, and so lowers the body's uric acid level. See above discussion in 6,c,iv regarding probenecid, and agent which is presently avaialble which also works to decrease the reabsorption of uric acid. RDEA594 has only had very early studies done19,and further studies are in progress with this agent alone and in combination with an agent that blocks the production of uric acid. An interesting finding is that this agent appears to increase the acidity of the urine, which has the potential to decrease the risk of uric acid kidney stones forming, since uric acid crystallizes out more readily in a less acidic environment. This agent can be taken once a day (as opposed to twice daily doses needed with probenecid) and to date no drug interactions with this agent have been reported (in contrast to several known interactions associated with probenecid).
e) BCX4208: This is a compound being studied as an alternative way to decrease the production of uric acid. It might be used alone, or together with a drug such as allopurinol or febuxostat in patients who otherwise could not have their uric acid level brought below 6. This agent works as a purine nucleoside phosphorylase inhibitor, a different mechanism than any of the medications to chronically lower uric acid described above.
Early studies suggest that this new mechanism is effective in lowering uric acid levels.20
8. Summary:
Gout is a common disease and appears to be becoming more common over time. We are fortunate to have a strong armamentarium against this condition, with newer agents in development. In view of the effectiveness of our treatments, it is important for a correct diagnosis to be made as early as possible, and therapy begun quickly when appropriate. Other conditions (e.g., pseudogout) which can mimic gout, should be definitively ruled out through crystal identification in joint fluid whenever possible. Non-medication treatments for gout are important, such as staying off the foot when it is inflamed and attending to diet both to reduce purine intake and to lose weight when indicated. For acute attacks of gout, a key is treating as quickly as possible and choosing a medication least likely to cause side-effects, with special attention to individual co-morbidities. For chronic prevention of gout, the essential message is that present treatments work in a huge majority of patients, and are generally well-tolerated. It is important for patients to understand the four stages of gout (See Figure 1) since the treatment of each is different. It is important for patients with gout to be carefully counseled to communicate any changes in the frequency of gout attacks to their practitioner. A primary care practitioner can often manage gout without a consultation with a rheumatologist, but consultation should be considered if the diagnosis is unclear, there is uncertainty as to whether or not to start uric acid-lowering medication, attacks continue to occur despite treatment, or possible medication side-effects are making treatment difficult.
9. Disclosures
Dr. Fields has served on the Gout Advisory Board for Takeda Pharmaceuticals, which markets the product febuxostat (Uloric®) and for URL Pharmaceuticals, which markets colchicine (Colcrys®). He receives no compensation related to sales or prescription of these medications.
10. More information:
Web resources:
1. Hospital for Special Surgery Website offers many links about gout, including a review of the ways the quality of care in gout can be evaluated. This site provides musculoskeletal information combining the skills of rheumatologists, orthopedists and musculoskeletal radiologists, with separate articles for a general audience and for medical professionals
2. MedLine Plus -- the NIH site for medical information for the public has valuable links on gout, including clinical trials, Spanish version, interactive tutorial, nutritional information, and listing of organizations which can help patients with gout. This site is a valuable resource on the spectrum of arthritic disorders.
3. Online pamphlet on gout from the Arthritis Foundation - a free printed copy of the pamphlet can also be ordered.
4. Information about the uric acid blood test from Lab Tests Online. This site is a good resource to learn about what your lab test results mean and why they are being done.
Books about gout (Annotated Bibliography):
1. Schneiter J. Gout Hater's Cookbook: Recipes Lower in Purines and Lower in Fat. (Reachment Publications; 2000) In addition to comprehensive lists of foods lower, relatively high, and highest in purines, this book offers nearly 100 low-purine recipes.
2. Schneiter J. Gout Hater's Cookbook II: The Low Purine Diet Cookbook. (Reachment Publications: 2001) More recipes from the same author. This book is useful since people often find the recommendations about low purine diets confusing and difficult to follow.
3. Wortmann RL, Schumacher RH and Becker M: Crystal-induced arthropathies: Gout, pseudogout & apatite-associated syndromes. Lavoisier Booksellers, Cachan Cedex, France, 2006. A detailed review of the various types of crystal-induced arthritis, targeted at a professional audience.
4. Emmerson B: Getting Rid of Gout: A Guide to Management and Prevention. Oxford University Press, London: 1996. A kidney specialist with special interest in gout explains the condition in detail for a lay audience.
5. Parker JN and Parker PM (Editors): The 2002 Official Patient’s SourceBook on Gout. A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002. A source covering a wide variety of sources of information about gout, including a glossary and research summaries.
6. Porter R and Rousseau GS: Gout: The Patrician Malady. Yale University Press, 2000. A socio-medical history of gout, including the famous figures who suffered from it, such as Benjamin Franklin and Thomas Jefferson.
Annotated References:
1 Wortmann RL. Effective management of gout: an analogy. Am J Med. 1998 Dec; 105(6):513-4. A review article that includes the "match" analogy to help patients understand the management of the various stages of gout, seeing uric acid as matches which can be “lit” (i.e. cause inflammation), “dampened” to decrease inflammation or removed from the joint.
2 Modified from Wallace, SL, et al: Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum., 20:895, 1977.
3 Baker et al: Serum uric acid and cardiovascular disease: Recent developments, and where do they leave us? Am J Med, 118:816-26, 2005. A review article concluding that uric acid is an independent risk factor for coronary disease.
4 Shoji et al: A retrospective study of the relationship between serum urate level and recurrent attacks of gouty arthritis: evidence for reduction of recurrent gouty arthritis with antihyperuricemic therapy. Arthritis Rheum, 51(3):321-5, 2004. This is one among a group of studies demonstrating the benefit of keeping uric acid below 6.0 in gout patients.
5 Choi HK et al: Purine-rich foods, dairy and protein intake, and the risk of gout in men. New Engl J Med, (11):1093-103, 2004. This article emphasizes the finding that red meat and shellfish increase gout risk while low-fat dairy intake seems to decrease it.
6 Choi HK et al: Alcohol intake and risk of incident gout in men: a prospective study. Lancet, 363(9417):1277-81, 2004. This article pinpoints beer as being a particular risk factor for gout.
7 Saag KG and Choi H: Epidemiology, risk factors, and lifestyle modifications for gout. Arthritis Res Ther 8 Suppl 1:S2, 2006. This article reviews lifestyle modifications that can influence gout risk, including weight loss, alcohol and diet.
8 Drenth J and van der Meer J: The Inflammasome — A Linebacker of Innate Defense. N Engl J Med 355:730-732, 2006. A review of a recently recognized pathway by which colchicine inhibits the inflammatory process of gout.
9 Singer JZ, Wallace SL: The allopurinol hypersensitivity syndrome: Unnecessary morbidity and mortality. Arthritis Rheum 29:82-6, 1986. This article stresses the importance of kidney abnormality as a risk factor in allopurinol hypersensitivity, and the importance of reducing allopurinol dose in patients with kidney dysfunction and of making sure that only patients who meet appropriate criteria get treated with allopurinol.
10 Dalbeth N and Stamp L. Allopurinol Dosing in Renal Impairment: Walking the Tightrope Between Adequate Urate Lowering and Adverse Events. Seminars in Dialysis 20:5, 391-395, 2007. This review emphasizes that it has not been proven that severe allopurinol allergic reactions relate to dose or that they are more common in patients with kidney problems. The authors also stress that keeping doses of allopurinol too low often leads to inadequate control of uric acid levels.
11 Fam AG, Dunne SM, Iazzetta J, et al. Efficacy and safety of desensitization to allopurinol following cutaneous reactions. Arthritis Rheum 44:231, 2001. This article reviews a regimen of oral desensitization to allopurinol, which has had significant success with low risk.
12 Richette P et al: Rasburicase for Gout Not Treatable with Allopurinol: an Exploratory Study. J Rheum 34:10, 2093-2098, 2007. Intravenous uricase, an enzyme that breaks down uric acid, was tried on a once-a-month basis in a small group of patients, with some success but some signs of allergic reactions.
13Sundy JS et al: Reduction of Plasma Urate Levels Following Treatment With Multiple Doses of Pegloticase (Polyethylene Glycol–Conjugated Uricase) in Patients With Treatment-Failure Gout: Results of a Phase II Randomized Study. Arthritis Rheum 58:9, 2882-2891, 2008.
14Sundy JS et al: Efficacy and Safety of Intravenous Pegloticase (PGL) in treatment failure gout (TFG): Results from Gout-1 and Gout-2. European League Against Rheumatism Abstract THU0446, June 2009. Abstract from European League Against Rheumatism Meeting 2009
15 Baraf, HSB et al: Reduction of tophus size with pegloticase (PGL) in treatment failure gout (TFG): Results from Gout-1 and Gout-2, European League Against Rheumatism Abstract OP-0047, June 2009. Abstract from European League Against Rheumatism Meeting 2009
16 So A et al: A pilot study of IL-1 inhibition by anakinra in acute gout. Arthritis Research & Therapy 9(2):R28, 2007
17Terkeltaub R et al: The interleukin 1 inhibitor rilonacept in treatment of chronic gouty arthritis: results of a placebo-controlled, monosequence crossover, non-randomised, single-blind pilot study. Annals of Rheumatic Disease 68:1613-1617, 2009
18So A at al: Canakinumab (ACZ885) Vs. Triamcinolone Acetonide for Treatment of Acute Flares and Prevention of Recurrent Flares in Gouty Arthritis Patients Refractory to or Contraindicated to NSAIDs and/or Colchicine. American College of Rheumatology Abstract LB4, October 2009. Abstract from American College of Rheumatology Meeting, Oct. 2009
19Yeh N et al: RDEA594, a potential uric acid lowering agent through inhibition of uric acid reuptake, shows better pharmocokinetics than its prodrug, RDEA806, poster #28, American College of Rheumatology Meeting, October 2008. Abstract from American College of Rheumatology Meeting 2008
20Fitz-patrick D et al: Abstract 150: Effects of a Purine Nucleoside Phosphorylase Inhibitor, BCX4208, on the Serum Uric Acid Concentrations in Patients with Gout. Abstract from the American College of Rheumatology Meeting November 2010.
Source:
http://knol.google.com/k/gout#
http://knol.google.com/k/gout#
Wednesday, November 23, 2011
Acne - What is acne? What are the best products to use for my acne?
Author:
Diane Thiboutot
Professor of Dermatology
Penn State University, Hershey, PA
Last Update on: 28 July 2008
What is acne?
Acne is a skin condition that affects the hair follicles (pores) of the face, chest, and back. Acne can vary in severity. In mild cases of acne, there are a few blackheads (open comedones) or whiteheads (closed comedones) with a few red or inflamed bumps (papules) and red or inflamed bumps with pus on the surface (pustules). In moderate acne, there are more blackheads and whiteheads and increasing numbers of papules and pustules. Severe acne can be associated with tender red cysts and nodules that can often be accompanied by scarring. The whiteheads, blackheads, papules, pustules, cysts, and nodules are called “acne lesions.” [See Figure 1].
Acne can affect almost anyone, but it is often thought to be a condition that just affects teenagers. Although the majority of people with acne (85%) are between the ages of 12 and 18, acne often affects adults and sometimes can affect newborns or infants. During adolescence, acne affects men and women equally but is more prevalent in adult women.
How do acne lesions develop?
Acne starts out underneath the skin where the cells that line the pore become sticky and do not move out of the pore onto the skin surface like normal cells. This results in a microscopic acne lesion called the “microcomedo” that cannot be seen with the naked eye. This microcomedo can turn into any one of the types of acne lesions (whiteheads, blackheads, papules, pustules, cysts). The process of a microcomedo turning into a visible acne lesion can take several weeks. Most acne treatments are designed to prevent microcomedoes from forming and developing into other acne lesions. That is why it is important to apply acne medications to all areas of the skin where acne can develop and not just on the acne lesion itself. Unlike treatments for other conditions, acne treatment can sometimes take several weeks to see improvement, because it is preventing the formation of microcomedoes beneath the skin and their further progression into a visible acne lesion.
What is happening in the skin to cause acne?
Each of 4 factors plays a role in the development of acne, but the exact sequence of events that leads to the development of acne is not known. [1] [Figure 2]
Factor 1. The cells that line the pore don’t readily move out onto the surface of the skin (this is called follicular hyperkeratinization, not follicular plugging, because the pore still has an opening).
Factor 2. The Propionibacterium acnes (P. acnes) bacteria in the skin secrete substances into the pore and the surrounding skin that induce inflammation (redness).
Factor 3. Oil (sebum) production by the oil gland (sebaceous gland) is increased, and it provides a good environment to support the growth of the P. acnes bacteria.
Factor 4. Inflammation: White blood cells that fight off infection are called into the skin near the pore by chemical signals originating from cells or bacteria within the pore. Some studies suggest that the movement of these cells towards the pore may be the first step in starting the acne process. The signal that calls the white blood cells to this area is not yet known. These white blood cells can secrete substances that induce inflammation, in addition to the inflammation induced by the P. acnes bacteria. The very red, sore acne papules or nodules can develop if the lining of the pore ruptures beneath the skin. When this happens, the inflammation and tenderness of the skin greatly intensifies. Sometimes this process happens on its own when the pore becomes enlarged with dead cells, oil, and bacteria. Picking or squeezing at acne can also cause the pore to rupture under the skin, which makes the redness or inflammation worse and can increase the risk of scarring.
What causes my skin to develop acne and what does not?
Many people have various beliefs and perceptions regarding the cause of acne [2]. It is only natural for people to think that their acne results from something they did or didn’t do, something they ate or didn’t eat, or something that they came in contact with, etc. In reality, acne happens for reasons that for the most part are out of our control. We can’t control changes in the cells of our pores, the fact that P. acnes lives on the skin, or the fact that our oil glands produce oil. As young people become teenagers, normal hormones in the body cause the oil glands to grow and secrete more oil on the face, chest, back, and scalp. The P. acnes bacteria live on the skin of teenagers and adults who have acne, and also on the skin of those not affected by acne. Here are some common questions about acne:
1. Do I have acne because I don’t wash my face enough?
No, the changes in the cells of the pores occur too deep in the pore to be affected by vigorous washing or scrubbing. In fact, vigorous washing or scrubbing serves more to aggravate acne than to help it. Gentle face washing to remove surface oils 2 or 3 times a day is recommended to improve the oily appearance of the skin, but face washing will not prevent acne from forming.
2. Do I have acne because I eat fatty foods, sugary foods (including chocolate), drink milk, or eat meat?
Most studies suggest that individual foods do not cause acne. Recently some studies suggest that diets low in refined sugars and sugar-containing foods (a low glycemic index diet) may be better for acne [3]. Some studies suggest that there could be a link between acne and milk, but there is no direct evidence for this. Milk contains calcium that is especially important for bone development in young people. Any diet where milk is eliminated or reduced would need to have alternative sources of calcium. Some people are concerned about hormones in meats and other foods. There have been no studies to link these foods to the development of acne.
3. Will the sun make my acne better?
Some people feel that their acne is better during the summer. This may be due to the fact that oftentimes, teenagers (and adults) may be less stressed during the summer, away from school or on vacation. Many people’s moods improve in sunny environments. These potential benefits can still be achieved while protecting skin health by using a sunscreen or other protective measures.
When will my acne go away?
For reasons that we do not understand, most teenagers affected by acne (boys in particular) notice that their acne starts to go away as they get into their 20s. For some girls, acne can persist or even develop for the first time in their 20s or later. It is thought that in adulthood, hormones influence acne in women more than in men. This may go against what one would think, since men have higher levels of acne-causing hormones, but it seems that women’s skin is more sensitive to hormones when it comes to developing acne. Some researchers think that the peak acne years (ages 12-18) coincide with the peak levels of a different hormone called insulin-like growth factor-1 (IGF-1), that regulates growth [4]. Levels of IGF-1 start to decline as people get into their 20s when the growth spurt stops. Whether the decline in IGF-1 accounts for the decline in acne at this age is not certain.
Will my acne leave scars?
The best way to avoid acne scarring is to avoid picking or squeezing acne lesions and to seek appropriate care for your acne before it leads to scarring. There is a lot of variation in the way that people’s skin reacts to having acne. It may take up to a year before a person can tell what kind of marks or scars could be left by their acne. As soon as an acne lesion heals, many people can have flat marks (level with the skin) that can be red, pink, purple, brown, dark brown, or black. These are called "postinflammatory macules" [Figure 1]. In most cases, if a person hasn’t picked or squeezed at their acne, these darker areas will lighten over time and won’t leave a permanent mark or scar. If someone’s acne is changing the contour of their skin leaving deep marks (beneath the surface contour of the face), this type of acne can heal with permanent scarring. Again, it takes almost up to a year before the skin fully heals. If after this time there are still depressed scars or other marks, these may be permanent.
What can I do about my acne?
Skin health benefits from a healthy lifestyle that includes a balanced diet that contains fruits, vegetables, and whole grains with limited refined sugars in addition to exercise, adequate sleep, and management of stress. Beginning to lead a healthy lifestyle as a teenager can have long-term benefits into adulthood. Proper skin care is geared to the type of skin that you have. In all cases it is important to cleanse the skin gently and avoid unnecessary rubbing or scrubbing of the acne. Using a soft washcloth or just the fingers is best. If the skin is oily, mild soaps or acne washes work well to remove the surface oils. If the skin is dry, gentle cleansing should be followed by use of a moisturizer. It is a good idea to consider a moisturizer that contains a sunscreen. Some people are concerned that moisturizers or other makeup could cause or aggravate acne. In most cases, this is not true. Most products from major companies are now tested in advance to show that they are noncomedogenic (don’t cause acne). Some people have used the strips designed to remove debris from the pores. There is no harm with gentle use of these strips, which some people feel improves the appearance of their skin.
What are the best products to use for my acne?
The best over-the-counter ingredient for acne is benzoyl peroxide. It is the most potent agent available to kill the P. acnes bacteria and should be the first place to start in looking for an over-the-counter acne treatment. Benzoyl peroxide is found in some acne cleansers, acne bar soaps, acne creams and gels, and in some of the popular products advertised on television. Since some products change their ingredients from time to time, the best way to find a benzoyl peroxide–containing product is to read the fine print—the list of ingredients on the back of the container or package. A small percentage of people may be allergic to benzoyl peroxide, as evidenced by excess redness, itching or peeling of the skin following its use. In these cases, benzoyl peroxide should be avoided. Salicylic acid is also a beneficial over-the-counter acne ingredient, and it is found in many products and in makeup designed for people with acne. Again keep in mind, all acne products work best when applied to the entire affected area, not just the acne lesions themselves. Spot treatment alone shortchanges the rest of your face. Keep in mind that benzoyl peroxide can bleach clothing, towels, and sometimes hair, so it is important to properly rinse off benzoyl peroxide washes from the chest and back and not to apply it too close to the hairline.
When should I see a doctor?
If you have used a benzoyl peroxide containing product for 6-8 weeks and there is no improvement in your acne, if your acne is scarring, or if your acne is severely affecting your self-esteem or ability to interact with others, you should see a doctor for acne treatment.
What type of doctor should I see?
Doctors that specialize in the treatment of skin conditions are called dermatologists, but many doctors treat acne including family physicians, pediatricians, internists, and others. In some cases, your primary care physician (family physician, pediatrician, or internist) can treat your acne or refer you to a dermatologist if you need additional treatment. Listings of dermatologists in your area can be found on the web site for the American Academy of Dermatology (www.aad.org).
What should I expect when I see a doctor for my acne?
Most doctors will want to know when your acne started, what you are currently using for your acne, what you have used in the past, and how you feel about having acne. For women, your doctor will also want to know if your menstrual periods are regular and if your acne flares with your menstrual periods. Doctors will visually examine your face, chest, and back to determine the extent of your acne, what types of acne lesions you have, and if you have signs of acne scarring. Doctors will usually then make recommendations for your skin care, give prescriptions to help clear the acne and in some cases discuss office treatments for your acne.
What types of prescription medications are used for acne? [5,6]
Prescription acne medications can be divided into topical treatments (such as washes, creams, lotions, gels) and oral treatments (such as antibiotic pills). More often that not, you may receive more than one prescription for your acne. This is because the different acne medications target one or more of the 4 factors that cause acne discussed above. Topical (applied to the skin) treatments include benzoyl peroxide washes, creams, gels, and lotions; topical antibiotics such as clindamycin or erythromycin; combination products containing both benzoyl peroxide and a topical antibiotic such as clindamycin (Duac, Benzaclin); topical retinoids such as tretinoin (Retin A and others), adapalene (Differin), and tazarotene (Tazorac); or combinations of tretinoin and clindamycin (Ziana). Benzoyl peroxide and topical antibiotics can kill the P. acnes bacteria. Topical retinoids can reverse the changes in the cells lining the pores and prevent the formation of the microcomedo. They can also reduce inflammation in acne. The combination products target multiple factors that cause acne.
Oral (taken by mouth) medications for acne include antibiotics such as tetracycline, doxycycline, or minocycline; hormonal therapies such as oral contraceptives; and isotretinoin (Accutane and others). Oral antibiotics work to kill the P. acnes bacteria and reduce inflammation. Oral contraceptives can be used to reduce the effects of hormones on acne in women. Isotretinoin is the most potent drug for acne that affects all 4 factors that cause this condition. It is generally taken for about 20 weeks. Isotretinoin can have serious side effects (see below) and its use requires close monitoring.
What should I expect from my acne treatment and how fast does it work?
Your doctor should discuss with you what to expect from your treatment in terms of possible side effects, the time it takes for the medication to work, how it should be applied or taken and how often, etc. The most common side effects from topical acne treatment are redness, dryness, scaling, or peeling of the skin. In most cases, these effects resolve after a couple of weeks. Regular use of a moisturizer helps to reduce these potential side effects. The most common side effects of oral antibiotics used for acne are allergic reactions (hives, rashes, swelling), stomach upset, potential sun sensitivity, or headache with some antibiotics. If there is concern about an allergic reaction, the medication should be stopped and you should contact your doctor. Hormonal therapies can be associated with an increased risk of blot clots in some patients. Isotretinoin can cause birth defects if a woman becomes pregnant on therapy or within a month afterwards. There are strict guidelines in place regarding preventing pregnancy in women receiving isotretinoin. Reports of depression and suicide have occurred in patients treated with isotretinoin. As mentioned above, the use of isotretinoin requires close monitoring.
In general, it takes at least 6-8 weeks to notice the full effect of an acne treatment regimen, so it is best to continue to use the medication as prescribed until you see your doctor again for a follow-up evaluation of your acne and your progress. It is also best to apply topical medications to the whole affected area whether it is the face, chest, or back. As mentioned before, by applying the medication this way, you’ll be helping to prevent the development of acne, rather than chasing after acne that has already had the chance to develop if you use spot treatment alone. When using topical acne treatment, more is not always better; you should use it as directed by your doctor, usually only a small amount. Application of medication to the back is often difficult. Help from someone else can be beneficial or use of a sponge with a handle to apply the medication to difficult to reach areas.
What types of office procedures are there for acne? [7]
There may be tremendous appeal in the prospect that acne can be kept under control with laser or light treatments or a chemical peels that could replace the need for taking pills, using washes, or applying topical medications. Unfortunately medical science is not quite there yet. Laser and light treatments for acne are approved by the US Food and Drug Administration (FDA). However, these are approved as devices (as opposed to drugs), and the criteria for approval differ between drugs and devices. Approval of a device requires less information about how effective the device is in treating acne compared with the amount of information required for drugs. As time goes on, laser and light therapies will continue to improve and more studies to compare them to standard acne medications will be conducted. In most cases, insurance does not cover laser and light treatments for acne, which can sometimes be expensive.
How long will I need treatment for my acne?
There is no one answer to this question, apart from “as long as the acne is active and bothersome.” The length of treatment for acne varies depending upon your family history of acne, the age at which you developed significant acne, your current age, and how your skin responds to treatment. Most acne occurs between the ages of 12 and 18. If someone has a family history of severe acne, it is possible that they could also develop severe acne that may require treatment as long as the acne is active possibly for several years. If someone has significant acne at an early age, they may require treatment throughout their teenage years. Adults with acne, women in particular, may need treatment for as long as their acne is active, which could be several years.
What can be done about my acne scarring? [8]
The best thing is to see a doctor to get the acne under control to prevent additional scarring. Although many treatments are available for acne scarring, there is no guarantee that the skin will be perfect after treatment for acne scars. Treatments for scarring can be performed by some dermatologists, plastic surgeons, and other physicians. Types of procedures include laser treatments, small skin grafts, release of scars from underlying skin, and chemical peels. Dermabrasion is no longer the standard treatment for acne scarring. It is best to get a consultation with a doctor to learn about the best treatments for your type of scarring and to get an estimate of the costs involved.
Is there new research on acne?
As medical science makes advances in understanding the factors that control inflammation, infection, and lipid metabolism in the body and in skin diseases, there are more opportunities to unravel the exact sequence of events leading to the development of acne. Research on acne and skin disease is supported by the US government (The National Institutes of Health, National Institute of Arthritis, Musculoskeletal and Skin Diseases www.niams.nih.gov), the Dermatology Foundation (www.dermatologyfoundation.org), the American Acne and Rosacea Society (www.acnesociety.org), international organizations, and many pharmaceutical and cosmetic companies.
Where can I get more information about acne?
Additional information about acne can be found at each of these websites:
The American Academy of Dermatology www.aad.org
National Institute of Arthritis, Musculoskeletal and Skin Diseases
•(English) www.niams.nih.gov/Health_info/acne
•(Spanish) www.niams.nih.gov/Portal_en_espanol/informacion_de_salud/acne
Medline Plus (National Library of Medicine) www.nlm.nih.gov/medlineplus/acne.html
References
1. Clarke SB. Nelson AM. George RE. Thiboutot DM.
Pharmacologic modulation of sebaceous gland activity: mechanisms and clinical applications. Dermatologic Clinics. 25(2):137-46, 2007
2. Tan JK. Vasey K. Fung KY. Beliefs and perceptions of patients with acne.
J Am Acad Dermatol 44(3):439-45, 2001
3. Smith RN. Mann NJ. Braue A. Makelainen H. Varigos GA.
The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: a randomized, investigator-masked, controlled trial. J Am Acad Dermatol 57(2):247-56, 2007
4. Rosenfield RL, Deplewski D. Role of androgens in the developmental biology of the pilosebaceous unit. Am J Medicine 98(1A):80S-88S, 1995
5. Strauss JS. Krowchuk DP. Leyden JJ. Lucky AW. Shalita AR. Siegfried EC. Thiboutot DM. Van Voorhees AS. Beutner KA. Sieck CK. Bhushan R. American Academy of Dermatology/American Academy of Dermatology Association. Guidelines of care for acne vulgaris management. J Am Acad Dermatol 56(4):651-63, 2007
6. Gollnick H. Cunliffe W. Berson D. Dreno B. Finlay A. Leyden JJ. Shalita AR. Thiboutot D. Global Alliance to Improve Outcomes in Acne. Management of acne: a report from a Global Alliance to Improve Outcomes in Acne. J Am Acad Dermatol 49(1 Suppl):S1-37, 2003
7. Taub A. Procedural treatments for acne vulgaris. Dermatol Surg 33: 1005-1026, 2007.
8. Goodman GJ and Baron JA. The management of postacne scarring. Dermatol Surg 33: 1175-1188, 2007
Diane Thiboutot
Professor of Dermatology
Penn State University, Hershey, PA
Last Update on: 28 July 2008
What is acne?
Acne is a skin condition that affects the hair follicles (pores) of the face, chest, and back. Acne can vary in severity. In mild cases of acne, there are a few blackheads (open comedones) or whiteheads (closed comedones) with a few red or inflamed bumps (papules) and red or inflamed bumps with pus on the surface (pustules). In moderate acne, there are more blackheads and whiteheads and increasing numbers of papules and pustules. Severe acne can be associated with tender red cysts and nodules that can often be accompanied by scarring. The whiteheads, blackheads, papules, pustules, cysts, and nodules are called “acne lesions.” [See Figure 1].
Acne can affect almost anyone, but it is often thought to be a condition that just affects teenagers. Although the majority of people with acne (85%) are between the ages of 12 and 18, acne often affects adults and sometimes can affect newborns or infants. During adolescence, acne affects men and women equally but is more prevalent in adult women.
How do acne lesions develop?
Acne starts out underneath the skin where the cells that line the pore become sticky and do not move out of the pore onto the skin surface like normal cells. This results in a microscopic acne lesion called the “microcomedo” that cannot be seen with the naked eye. This microcomedo can turn into any one of the types of acne lesions (whiteheads, blackheads, papules, pustules, cysts). The process of a microcomedo turning into a visible acne lesion can take several weeks. Most acne treatments are designed to prevent microcomedoes from forming and developing into other acne lesions. That is why it is important to apply acne medications to all areas of the skin where acne can develop and not just on the acne lesion itself. Unlike treatments for other conditions, acne treatment can sometimes take several weeks to see improvement, because it is preventing the formation of microcomedoes beneath the skin and their further progression into a visible acne lesion.
What is happening in the skin to cause acne?
Each of 4 factors plays a role in the development of acne, but the exact sequence of events that leads to the development of acne is not known. [1] [Figure 2]
Factor 1. The cells that line the pore don’t readily move out onto the surface of the skin (this is called follicular hyperkeratinization, not follicular plugging, because the pore still has an opening).
Factor 2. The Propionibacterium acnes (P. acnes) bacteria in the skin secrete substances into the pore and the surrounding skin that induce inflammation (redness).
Factor 3. Oil (sebum) production by the oil gland (sebaceous gland) is increased, and it provides a good environment to support the growth of the P. acnes bacteria.
Factor 4. Inflammation: White blood cells that fight off infection are called into the skin near the pore by chemical signals originating from cells or bacteria within the pore. Some studies suggest that the movement of these cells towards the pore may be the first step in starting the acne process. The signal that calls the white blood cells to this area is not yet known. These white blood cells can secrete substances that induce inflammation, in addition to the inflammation induced by the P. acnes bacteria. The very red, sore acne papules or nodules can develop if the lining of the pore ruptures beneath the skin. When this happens, the inflammation and tenderness of the skin greatly intensifies. Sometimes this process happens on its own when the pore becomes enlarged with dead cells, oil, and bacteria. Picking or squeezing at acne can also cause the pore to rupture under the skin, which makes the redness or inflammation worse and can increase the risk of scarring.
What causes my skin to develop acne and what does not?
Many people have various beliefs and perceptions regarding the cause of acne [2]. It is only natural for people to think that their acne results from something they did or didn’t do, something they ate or didn’t eat, or something that they came in contact with, etc. In reality, acne happens for reasons that for the most part are out of our control. We can’t control changes in the cells of our pores, the fact that P. acnes lives on the skin, or the fact that our oil glands produce oil. As young people become teenagers, normal hormones in the body cause the oil glands to grow and secrete more oil on the face, chest, back, and scalp. The P. acnes bacteria live on the skin of teenagers and adults who have acne, and also on the skin of those not affected by acne. Here are some common questions about acne:
1. Do I have acne because I don’t wash my face enough?
No, the changes in the cells of the pores occur too deep in the pore to be affected by vigorous washing or scrubbing. In fact, vigorous washing or scrubbing serves more to aggravate acne than to help it. Gentle face washing to remove surface oils 2 or 3 times a day is recommended to improve the oily appearance of the skin, but face washing will not prevent acne from forming.
2. Do I have acne because I eat fatty foods, sugary foods (including chocolate), drink milk, or eat meat?
Most studies suggest that individual foods do not cause acne. Recently some studies suggest that diets low in refined sugars and sugar-containing foods (a low glycemic index diet) may be better for acne [3]. Some studies suggest that there could be a link between acne and milk, but there is no direct evidence for this. Milk contains calcium that is especially important for bone development in young people. Any diet where milk is eliminated or reduced would need to have alternative sources of calcium. Some people are concerned about hormones in meats and other foods. There have been no studies to link these foods to the development of acne.
3. Will the sun make my acne better?
Some people feel that their acne is better during the summer. This may be due to the fact that oftentimes, teenagers (and adults) may be less stressed during the summer, away from school or on vacation. Many people’s moods improve in sunny environments. These potential benefits can still be achieved while protecting skin health by using a sunscreen or other protective measures.
When will my acne go away?
For reasons that we do not understand, most teenagers affected by acne (boys in particular) notice that their acne starts to go away as they get into their 20s. For some girls, acne can persist or even develop for the first time in their 20s or later. It is thought that in adulthood, hormones influence acne in women more than in men. This may go against what one would think, since men have higher levels of acne-causing hormones, but it seems that women’s skin is more sensitive to hormones when it comes to developing acne. Some researchers think that the peak acne years (ages 12-18) coincide with the peak levels of a different hormone called insulin-like growth factor-1 (IGF-1), that regulates growth [4]. Levels of IGF-1 start to decline as people get into their 20s when the growth spurt stops. Whether the decline in IGF-1 accounts for the decline in acne at this age is not certain.
Will my acne leave scars?
The best way to avoid acne scarring is to avoid picking or squeezing acne lesions and to seek appropriate care for your acne before it leads to scarring. There is a lot of variation in the way that people’s skin reacts to having acne. It may take up to a year before a person can tell what kind of marks or scars could be left by their acne. As soon as an acne lesion heals, many people can have flat marks (level with the skin) that can be red, pink, purple, brown, dark brown, or black. These are called "postinflammatory macules" [Figure 1]. In most cases, if a person hasn’t picked or squeezed at their acne, these darker areas will lighten over time and won’t leave a permanent mark or scar. If someone’s acne is changing the contour of their skin leaving deep marks (beneath the surface contour of the face), this type of acne can heal with permanent scarring. Again, it takes almost up to a year before the skin fully heals. If after this time there are still depressed scars or other marks, these may be permanent.
What can I do about my acne?
Skin health benefits from a healthy lifestyle that includes a balanced diet that contains fruits, vegetables, and whole grains with limited refined sugars in addition to exercise, adequate sleep, and management of stress. Beginning to lead a healthy lifestyle as a teenager can have long-term benefits into adulthood. Proper skin care is geared to the type of skin that you have. In all cases it is important to cleanse the skin gently and avoid unnecessary rubbing or scrubbing of the acne. Using a soft washcloth or just the fingers is best. If the skin is oily, mild soaps or acne washes work well to remove the surface oils. If the skin is dry, gentle cleansing should be followed by use of a moisturizer. It is a good idea to consider a moisturizer that contains a sunscreen. Some people are concerned that moisturizers or other makeup could cause or aggravate acne. In most cases, this is not true. Most products from major companies are now tested in advance to show that they are noncomedogenic (don’t cause acne). Some people have used the strips designed to remove debris from the pores. There is no harm with gentle use of these strips, which some people feel improves the appearance of their skin.
What are the best products to use for my acne?
The best over-the-counter ingredient for acne is benzoyl peroxide. It is the most potent agent available to kill the P. acnes bacteria and should be the first place to start in looking for an over-the-counter acne treatment. Benzoyl peroxide is found in some acne cleansers, acne bar soaps, acne creams and gels, and in some of the popular products advertised on television. Since some products change their ingredients from time to time, the best way to find a benzoyl peroxide–containing product is to read the fine print—the list of ingredients on the back of the container or package. A small percentage of people may be allergic to benzoyl peroxide, as evidenced by excess redness, itching or peeling of the skin following its use. In these cases, benzoyl peroxide should be avoided. Salicylic acid is also a beneficial over-the-counter acne ingredient, and it is found in many products and in makeup designed for people with acne. Again keep in mind, all acne products work best when applied to the entire affected area, not just the acne lesions themselves. Spot treatment alone shortchanges the rest of your face. Keep in mind that benzoyl peroxide can bleach clothing, towels, and sometimes hair, so it is important to properly rinse off benzoyl peroxide washes from the chest and back and not to apply it too close to the hairline.
When should I see a doctor?
If you have used a benzoyl peroxide containing product for 6-8 weeks and there is no improvement in your acne, if your acne is scarring, or if your acne is severely affecting your self-esteem or ability to interact with others, you should see a doctor for acne treatment.
What type of doctor should I see?
Doctors that specialize in the treatment of skin conditions are called dermatologists, but many doctors treat acne including family physicians, pediatricians, internists, and others. In some cases, your primary care physician (family physician, pediatrician, or internist) can treat your acne or refer you to a dermatologist if you need additional treatment. Listings of dermatologists in your area can be found on the web site for the American Academy of Dermatology (www.aad.org).
What should I expect when I see a doctor for my acne?
Most doctors will want to know when your acne started, what you are currently using for your acne, what you have used in the past, and how you feel about having acne. For women, your doctor will also want to know if your menstrual periods are regular and if your acne flares with your menstrual periods. Doctors will visually examine your face, chest, and back to determine the extent of your acne, what types of acne lesions you have, and if you have signs of acne scarring. Doctors will usually then make recommendations for your skin care, give prescriptions to help clear the acne and in some cases discuss office treatments for your acne.
What types of prescription medications are used for acne? [5,6]
Prescription acne medications can be divided into topical treatments (such as washes, creams, lotions, gels) and oral treatments (such as antibiotic pills). More often that not, you may receive more than one prescription for your acne. This is because the different acne medications target one or more of the 4 factors that cause acne discussed above. Topical (applied to the skin) treatments include benzoyl peroxide washes, creams, gels, and lotions; topical antibiotics such as clindamycin or erythromycin; combination products containing both benzoyl peroxide and a topical antibiotic such as clindamycin (Duac, Benzaclin); topical retinoids such as tretinoin (Retin A and others), adapalene (Differin), and tazarotene (Tazorac); or combinations of tretinoin and clindamycin (Ziana). Benzoyl peroxide and topical antibiotics can kill the P. acnes bacteria. Topical retinoids can reverse the changes in the cells lining the pores and prevent the formation of the microcomedo. They can also reduce inflammation in acne. The combination products target multiple factors that cause acne.
Oral (taken by mouth) medications for acne include antibiotics such as tetracycline, doxycycline, or minocycline; hormonal therapies such as oral contraceptives; and isotretinoin (Accutane and others). Oral antibiotics work to kill the P. acnes bacteria and reduce inflammation. Oral contraceptives can be used to reduce the effects of hormones on acne in women. Isotretinoin is the most potent drug for acne that affects all 4 factors that cause this condition. It is generally taken for about 20 weeks. Isotretinoin can have serious side effects (see below) and its use requires close monitoring.
What should I expect from my acne treatment and how fast does it work?
Your doctor should discuss with you what to expect from your treatment in terms of possible side effects, the time it takes for the medication to work, how it should be applied or taken and how often, etc. The most common side effects from topical acne treatment are redness, dryness, scaling, or peeling of the skin. In most cases, these effects resolve after a couple of weeks. Regular use of a moisturizer helps to reduce these potential side effects. The most common side effects of oral antibiotics used for acne are allergic reactions (hives, rashes, swelling), stomach upset, potential sun sensitivity, or headache with some antibiotics. If there is concern about an allergic reaction, the medication should be stopped and you should contact your doctor. Hormonal therapies can be associated with an increased risk of blot clots in some patients. Isotretinoin can cause birth defects if a woman becomes pregnant on therapy or within a month afterwards. There are strict guidelines in place regarding preventing pregnancy in women receiving isotretinoin. Reports of depression and suicide have occurred in patients treated with isotretinoin. As mentioned above, the use of isotretinoin requires close monitoring.
In general, it takes at least 6-8 weeks to notice the full effect of an acne treatment regimen, so it is best to continue to use the medication as prescribed until you see your doctor again for a follow-up evaluation of your acne and your progress. It is also best to apply topical medications to the whole affected area whether it is the face, chest, or back. As mentioned before, by applying the medication this way, you’ll be helping to prevent the development of acne, rather than chasing after acne that has already had the chance to develop if you use spot treatment alone. When using topical acne treatment, more is not always better; you should use it as directed by your doctor, usually only a small amount. Application of medication to the back is often difficult. Help from someone else can be beneficial or use of a sponge with a handle to apply the medication to difficult to reach areas.
What types of office procedures are there for acne? [7]
There may be tremendous appeal in the prospect that acne can be kept under control with laser or light treatments or a chemical peels that could replace the need for taking pills, using washes, or applying topical medications. Unfortunately medical science is not quite there yet. Laser and light treatments for acne are approved by the US Food and Drug Administration (FDA). However, these are approved as devices (as opposed to drugs), and the criteria for approval differ between drugs and devices. Approval of a device requires less information about how effective the device is in treating acne compared with the amount of information required for drugs. As time goes on, laser and light therapies will continue to improve and more studies to compare them to standard acne medications will be conducted. In most cases, insurance does not cover laser and light treatments for acne, which can sometimes be expensive.
How long will I need treatment for my acne?
There is no one answer to this question, apart from “as long as the acne is active and bothersome.” The length of treatment for acne varies depending upon your family history of acne, the age at which you developed significant acne, your current age, and how your skin responds to treatment. Most acne occurs between the ages of 12 and 18. If someone has a family history of severe acne, it is possible that they could also develop severe acne that may require treatment as long as the acne is active possibly for several years. If someone has significant acne at an early age, they may require treatment throughout their teenage years. Adults with acne, women in particular, may need treatment for as long as their acne is active, which could be several years.
What can be done about my acne scarring? [8]
The best thing is to see a doctor to get the acne under control to prevent additional scarring. Although many treatments are available for acne scarring, there is no guarantee that the skin will be perfect after treatment for acne scars. Treatments for scarring can be performed by some dermatologists, plastic surgeons, and other physicians. Types of procedures include laser treatments, small skin grafts, release of scars from underlying skin, and chemical peels. Dermabrasion is no longer the standard treatment for acne scarring. It is best to get a consultation with a doctor to learn about the best treatments for your type of scarring and to get an estimate of the costs involved.
Is there new research on acne?
As medical science makes advances in understanding the factors that control inflammation, infection, and lipid metabolism in the body and in skin diseases, there are more opportunities to unravel the exact sequence of events leading to the development of acne. Research on acne and skin disease is supported by the US government (The National Institutes of Health, National Institute of Arthritis, Musculoskeletal and Skin Diseases www.niams.nih.gov), the Dermatology Foundation (www.dermatologyfoundation.org), the American Acne and Rosacea Society (www.acnesociety.org), international organizations, and many pharmaceutical and cosmetic companies.
Where can I get more information about acne?
Additional information about acne can be found at each of these websites:
The American Academy of Dermatology www.aad.org
National Institute of Arthritis, Musculoskeletal and Skin Diseases
•(English) www.niams.nih.gov/Health_info/acne
•(Spanish) www.niams.nih.gov/Portal_en_espanol/informacion_de_salud/acne
Medline Plus (National Library of Medicine) www.nlm.nih.gov/medlineplus/acne.html
References
1. Clarke SB. Nelson AM. George RE. Thiboutot DM.
Pharmacologic modulation of sebaceous gland activity: mechanisms and clinical applications. Dermatologic Clinics. 25(2):137-46, 2007
2. Tan JK. Vasey K. Fung KY. Beliefs and perceptions of patients with acne.
J Am Acad Dermatol 44(3):439-45, 2001
3. Smith RN. Mann NJ. Braue A. Makelainen H. Varigos GA.
The effect of a high-protein, low glycemic-load diet versus a conventional, high glycemic-load diet on biochemical parameters associated with acne vulgaris: a randomized, investigator-masked, controlled trial. J Am Acad Dermatol 57(2):247-56, 2007
4. Rosenfield RL, Deplewski D. Role of androgens in the developmental biology of the pilosebaceous unit. Am J Medicine 98(1A):80S-88S, 1995
5. Strauss JS. Krowchuk DP. Leyden JJ. Lucky AW. Shalita AR. Siegfried EC. Thiboutot DM. Van Voorhees AS. Beutner KA. Sieck CK. Bhushan R. American Academy of Dermatology/American Academy of Dermatology Association. Guidelines of care for acne vulgaris management. J Am Acad Dermatol 56(4):651-63, 2007
6. Gollnick H. Cunliffe W. Berson D. Dreno B. Finlay A. Leyden JJ. Shalita AR. Thiboutot D. Global Alliance to Improve Outcomes in Acne. Management of acne: a report from a Global Alliance to Improve Outcomes in Acne. J Am Acad Dermatol 49(1 Suppl):S1-37, 2003
7. Taub A. Procedural treatments for acne vulgaris. Dermatol Surg 33: 1005-1026, 2007.
8. Goodman GJ and Baron JA. The management of postacne scarring. Dermatol Surg 33: 1175-1188, 2007
POISON IVY and POISON OAK - A Concise Summary of Diagnosis and Treatment
Author
Adam Goldstein, MD, MPH
Physician
Chapel Hill, NC
Most people in the U.S. have either gotten poison ivy or poison oak at one point in time, or they know someone who has gotten it. Poison ivy and poison oak cause tremendous misery to those who get it and to their family members who endure their loved one’s itching. Even doctors often fail to recognize the severity of the condition, resulting in needless delays in diagnosis and effective treatment. Finally, many beliefs exist about poison ivy, such as that scratching makes it spread or that it is contagious, most of which are wrong!
The purpose of this article is to give accurate information about poison ivy and poison oak, their causes and treatment, for parents and other adults with a need to know what to do and what not to do about someone they know with poison ivy or poison oak.
WHAT EXACTLY ARE POISON IVY AND POISON OAK?
Both poison ivy and poison oak come from the plant family called Toxicodendron. The plants contain a chemical poison called urushiol that is highly irritating to human skin. The condition that poison ivy and poison oak cause is called “allergic contact dermatitis.” It’s called allergic because the plant causes the skin to become severely inflamed and itch. You cannot get it unless you actually come in contact with the poison. Dermatitis means severe reaction or inflammation (-itis) in the layer of the skin called the dermis. In other words, these types of toxic or skin poisons cause an allergic skin reaction when you come in contact with them.
WHAT IS THE DIFFERENCE BETWEEN POISON IVY, POISON OAK, AND POISON SUMAC?
Actually, very little difference exists between all forms of poison ivy and poison oak. The difference comes from the slightly different type of Toxicodendron plant family each comes from. Poison sumac is another form of Toxicodendron plant family that causes an allergic contact dermatitis. All forms of this family have similar symptoms and are treated virtually the same.
WHO GETS POISON IVY AND POISON OAK?
The simple answer is almost everyone. Up to 75% of people who come in contact with the leaves, vines, or oil from the plant will have a skin reaction. Each year in the U.S. alone, tens of millions adults and children get poison ivy or poison oak. It is found in almost every state (at altitudes less than 4000 feet and in places that receive at least several inches of rain each year).
While it is true that some individuals will not get poison ivy or poison oak when they come into contact with the plant, most will. After repeated exposure, most will get skin irritation even more easily, because the skin becomes highly sensitive to the poison. People who go outside and work in gardens, who have outdoor occupations, and who take hikes in the woods are particularly likely to get poison ivy. Although people are much more likely to get poison ivy and poison oak during the summer months, cases can occur at any time of year if someone comes into contact with the plants.
HOW EXACTLY DO YOU “GET” POISON IVY AND POISON OAK?
The way most everyone gets poison ivy or poison oak is by touching the plant itself (see figure A below). Some people get confused with plants like the 'Virginia Creeper' that look similar to poison ivy and poison oak, but they have five leaves, not three, and are harmless when touched (See Figure B below). Since most people actually touch the plants while hiking or gardening, the chemical poison in the plants affects them everywhere the plant has touched them. If they touched the plant with their hands, they will get poison ivy on their hands. If the plant touched their legs and thighs while hiking, they will get the disease on their legs and thighs. If they are sweating, and they wipe their face and neck with their hands that have just touched the plant, they will likely get poison ivy on their face and neck. More rarely, people can get a severe case of poison ivy all over their body or face by exposure to the “fumes” when the plant is burned.
WHAT ARE THE SYMPTOMS OF POISON IVY AND POISON OAK?
Almost everyone who has ever gotten poison ivy or poison oak can tell a doctor that their symptoms are itching, itching, and more itching. Frequently, the symptoms start out as very mild itching on a finger, hand, or forehead. You may not even see anything. You just start scratching or rubbing the skin. After a few hours or even a day, you notice that the skin where you have been rubbing and scratching is red and some small bumps are appearing. You also notice that several parts of the body seem to have the same thing happening.
The bumps of poison ivy and poison oak are usually small and red. At first, the bumps may appear isolated to different places of the body. Then they seem to come together into larger areas, often following “lines”, as if someone took a feather and drew it across the skin. This is in fact what has happened, as the leaf of the plant has drawn across the skin.
In fact, wherever the plant touched the skin, the rash will break out. Your skin, however, reacts at different times. This is important to know, because most people think that their poison ivy and oak are “spreading,” when in fact it is not. So, what may appear to you as spreading poison ivy is simply your skin reacting to the chemical poison at different times. The effect, however, is that you often cannot tell the full extent of poison ivy or poison oak simply by looking at what it looks like early on in the disease, in the first day or two. It will usually get worse. This is a really important piece of information to know, because your symptoms will also usually get worse.
As the condition gets worse, the small bumps come together and form groups of bumps called vesicles. These vesicles contain clear or honey-colored fluid with all kinds of cells that are reacting to the irritated skin. As you scratch more and more, the bumps and vesicles get more irritated and break open, forming crusts on the skin.
Often, people keep scratching these vesicles until they bleed. The reason is that the sensation of pain is less bothersome to most people than the symptoms of itching. Unfortunately, if you scratch your rash until it bleeds, it also means that you stand a chance of your rash getting infected with bacteria. In this case, you may need to take oral antibiotics. (See section on treatment below.)
HOW LONG WILL THE RASH LAST IF I DO NOTHING?
Most cases of poison ivy and poison oak will go away on their own within two or at most three weeks (See figure below). Some cases can last as long as a month. Many people do not recognize what the plant looks like, so they get repeated exposure and repeated outbreaks, particularly during the summer months.
HOW DO I KNOW IF I HAVE POISON IVY OR POISON OAK?
If you start itching in the summer, on several parts of your body, particularly your hands or arms or face, and then develop small red bumps that start to appear in streaky lines, with lots and lots of itching, then you may have poison ivy or poison oak, particularly if you were working or walking outdoors in the woods 1-2 days previously.
Many other diseases can look like poison ivy or poison oak initially, so it is not always easy to tell the difference, particularly early on in the process. Eczema (shownbelow) is a disease of dry skin that can cause itching over much of the body, but it is usually chronic and not acute. If poison ivy or poison oak occurs in someone who also has eczema, the skin irritation can be very great.
Poison ivy and poison oak can also look similar to some skin reactions to drugs. Allergies to other plants or even things like clothes, detergents, or latex, can have a similar appearance. Usually, allergies to most other items are symmetrical, that is, the rash looks fairly even on both sides of the body. In contrast, the rash of poison ivy and poison oak is usually not symmetrical, reflecting the rather chance locations that the plant has encountered the skin.
Finally, a disease called scabies, caused by a parasite, can also cause very severe itching of the skin, but it does not usually have vesicles that ooze fluid, and the distribution of scabies is often confined to the wrists, finger webs, underarms, waste, groin, ankles and toe webs.
IS POISON IVY OR POISON OAK CONTAGIOUS?
As mentioned earlier, you cannot get poison ivy from someone who has it, only from the exposure to the plant itself. Thus, if you touch someone else’s’ rash, you should not get the disease. Of course, why would you touch someone else’s rash, as it is their rash, not yours!
WILL I SPREAD POISON IVY ON MY BODY BY SCRATCHING IT?
The answer, as described above is no, no, and no. It may appear that way to you, but that is actually just where the plant originally touched your skin, and the skin reacts differently and at different times.
HOW DO I TREAT POISON IVY AND POISON OAK?
If you have poison ivy or poison oak limited to a small area, you can sometimes treat it by using creams that you can buy in your local drug store.
If the rash occurs on more than one arm and leg, if it occurs on your face, or if it causes you to scratch at all hours of the day or night, you probably want to talk to your doctor about getting a prescription medication called corticosteroids. You can get this medication as either a topical preparation to apply to your skin or pills you take by mouth.
Topical steroids prescribed by physicians come in many strengths, and you usually only need to apply them once or twice a day. They help but often times do not fully remove the itching, and once the full blown rash comes out, they are less effective.
For severe itching or disease that involves many parts of the body, doctors usually recommend oral corticosteroids, usually called prednisone. Prednisone is usually given at higher doses for the first several days and then the dose is lowered over 7-14 days. It is very important to take the prednisone pills exactly as your doctor directs. If you stop the prednisone too soon, the rash of poison ivy and poison oak will likely come back. Prednisone is highly effective in treating the rash and itching, and it can be taken usually only once a day.
Many over-the-counter lotions, creams, and ointments can help with itching. Some of these (Hytone, Cortaid, Cortisone, Aquanil HC, Dermtex) contain 0.5-1% hydrocortisone cream, a mild anti-inflammatory medication. Products that contain Calamine are soothing to the skin, and as they evaporate, the itch temporarily improves. Some products contain phenol, menthol, camphor or pramoxine that can ease itching temporarily. Brand names of these products include: Gold-Bond anti-itch cream, Tecnu rash relief spray, Calagel anti-itch gel, Pramoxine Anti-itch lotion, Dermoplast spray, Pramegel, Prax cream and lotion, Itch-X spray and gel, and Sarna cream and foam. Oatmeal baths, such as Aveeno, can also provide temporary relief.
Sometimes, an oral antihistamine (allergy pill), such as diphenhydramine, can also help lessen the itching. Topical antihistamines should be avoided however, as they can make the skin even more sensitive. You should ask your doctor about all these medications.
One of the best things you can do to ease the itching is put cold compresses on the rash. To do this, put a clean cloth in cool water, and then wring out the excess water. Burow’s solution is a medication (aluminum acetate) added to cool compresses that has a cooling and drying effect to decrease itching. One of the worst things you can do for the itching is to put heat on it, as this will simply cause it to become more irritated and itch more. You may notice that the itching worsens, for example, after you take a hot shower.
HOW CAN I AVOID GETTING POISON IVY OR OAK?
The best way to not get poison ivy and poison oak is to recognize the plant and avoid touching it if at all possible. The plants have a usual appearance as three-leaved groupings arising from a central red stem. Posion oak resembles leaves of an oak tree. The leaves of poison ivy are frequently quite shiny. An old rhyme is useful to remember: “Leaves of three, let it be”. Even when dried, the leaves can cause a rash if you touch them or the stem, so cutting down old poison ivy vines in the winter can still be problematic. If the leaves touch your pants, clothes, or gloves, make sure you wash the clothes or gloves thoroughly before wearing them again.
When hiking or gardening in areas with poison ivy, it is important to wear protective pants, long-sleeve shirt and even gloves. Do not burn poison ivy plants, as the fumes can cause a severe allergic reaction to those with sensitivity to the plant poison. Also, if you are hiking with a pet in an area with poison ivy, make sure you wash the pet after hiking to prevent the pet giving you the disease from exposure to the urushiol on the pet’s fur.
Some people who garden frequently in areas with lots of poison ivy may choose to use a product called IvyBlock, a lotion that contains Bentoquatam. This lotion may bind to urushiol and thus block the ability of urushiol to attach to the skin. It must be used at least 15 minutes before exposure to the plants, and it should not be used by children younger than seven years of age. It also must be reapplied after being exposed to the plants for more than four hours, and it leaves a clay-like residue on the skin after it dries.
Some people also consider using barrier creams that are about 60% effective in preventing poison ivy when applied liberally to the skin before being exposed. A study in 1992 from Duke University showed that products such as StokoGard barrier cream, Hollister Moisture Barrier cream or ointment, and Hydropel ointment are effective.
WHAT SHOULD I DO IF I TOUCH THE POISON IVY OR POISON OAK PLANT?
If you know that you have touched the plant and did not have gloves on, the very first thing you should do is immediately wash your hands with soap and water, or even wipe them down with rubbing alcohol followed by water. If you can do so within 5-10 minutes of exposure to the plant, you may be able to avoid getting the reaction. After 30 minutes, washing the skin is good, but you will likely still get the skin reaction and disease.
You can use several mild, over the counter detergent creams to cut down on the reaction you might get if you were not able to wash the skin in the first thirty minutes but you had significant exposure to poison ivy. One chemical that can decrease the reaction up to several hours after exposure is called Tecnu skin cleanser. You apply this cream for two minutes to places where you were exposed to the poison ivy or poison oak plant, and then wash with water. Goop hand cleaner in a gel, liquid or soap is another product designed to remove the oil resin from the skin. Finally, you can purchase a soap mixture of that combines ethoxlate and sodium lauroyl sarcosinate surfactants, called Zanfel, that can help remove urushiol in contact with the skin.
SHOULD I PUT BLEACH ON THE RASH?
Absolutely not! Using bleach on the skin is like putting a second poison on the skin. You will kill off several layers of skin, and your skin may hurt more than it itches for a while. Subsequently, you risk making the skin reaction much worse, including having infections of the skin.
CAN MY CHILD GO TO SCHOOL OR CAMP IF THEY HAVE POISON IVY OR POISON OAK?
Absolutely! Since poison ivy and poison oak are not contagious to others, no reason exists to keep children away from other children. Do not think, however, that teachers, school administrators or even other children will know all the information that you now know. You may need to educate them about the disease, or even get a doctor’s note saying that everything is okay.
WHAT ELSE DO I NEED TO KNOW?
If your rash does not get better, or if it worsens, you should see your doctor. It is also important to see your doctor if you develop a fever, if the rash covers a large area of your body, or if there is pus coming from the bumps on your skin. These symptoms may indicate that you need more than just over-the-counter treatments.
As mentioned above, sometimes other things can cause a severe itching rash, such as allergies to other substances. Your doctor can help determine what is causing the condition, and they will offer the best treatments available.
Source:
http://knol.google.com/k/poison-ivy-and-poison-oak#
http://knol.google.com/k/poison-ivy-and-poison-oak#
Adam Goldstein, MD, MPH
Physician
Chapel Hill, NC
Most people in the U.S. have either gotten poison ivy or poison oak at one point in time, or they know someone who has gotten it. Poison ivy and poison oak cause tremendous misery to those who get it and to their family members who endure their loved one’s itching. Even doctors often fail to recognize the severity of the condition, resulting in needless delays in diagnosis and effective treatment. Finally, many beliefs exist about poison ivy, such as that scratching makes it spread or that it is contagious, most of which are wrong!
The purpose of this article is to give accurate information about poison ivy and poison oak, their causes and treatment, for parents and other adults with a need to know what to do and what not to do about someone they know with poison ivy or poison oak.
WHAT EXACTLY ARE POISON IVY AND POISON OAK?
Both poison ivy and poison oak come from the plant family called Toxicodendron. The plants contain a chemical poison called urushiol that is highly irritating to human skin. The condition that poison ivy and poison oak cause is called “allergic contact dermatitis.” It’s called allergic because the plant causes the skin to become severely inflamed and itch. You cannot get it unless you actually come in contact with the poison. Dermatitis means severe reaction or inflammation (-itis) in the layer of the skin called the dermis. In other words, these types of toxic or skin poisons cause an allergic skin reaction when you come in contact with them.
WHAT IS THE DIFFERENCE BETWEEN POISON IVY, POISON OAK, AND POISON SUMAC?
Actually, very little difference exists between all forms of poison ivy and poison oak. The difference comes from the slightly different type of Toxicodendron plant family each comes from. Poison sumac is another form of Toxicodendron plant family that causes an allergic contact dermatitis. All forms of this family have similar symptoms and are treated virtually the same.
WHO GETS POISON IVY AND POISON OAK?
The simple answer is almost everyone. Up to 75% of people who come in contact with the leaves, vines, or oil from the plant will have a skin reaction. Each year in the U.S. alone, tens of millions adults and children get poison ivy or poison oak. It is found in almost every state (at altitudes less than 4000 feet and in places that receive at least several inches of rain each year).
While it is true that some individuals will not get poison ivy or poison oak when they come into contact with the plant, most will. After repeated exposure, most will get skin irritation even more easily, because the skin becomes highly sensitive to the poison. People who go outside and work in gardens, who have outdoor occupations, and who take hikes in the woods are particularly likely to get poison ivy. Although people are much more likely to get poison ivy and poison oak during the summer months, cases can occur at any time of year if someone comes into contact with the plants.
HOW EXACTLY DO YOU “GET” POISON IVY AND POISON OAK?
The way most everyone gets poison ivy or poison oak is by touching the plant itself (see figure A below). Some people get confused with plants like the 'Virginia Creeper' that look similar to poison ivy and poison oak, but they have five leaves, not three, and are harmless when touched (See Figure B below). Since most people actually touch the plants while hiking or gardening, the chemical poison in the plants affects them everywhere the plant has touched them. If they touched the plant with their hands, they will get poison ivy on their hands. If the plant touched their legs and thighs while hiking, they will get the disease on their legs and thighs. If they are sweating, and they wipe their face and neck with their hands that have just touched the plant, they will likely get poison ivy on their face and neck. More rarely, people can get a severe case of poison ivy all over their body or face by exposure to the “fumes” when the plant is burned.
WHAT ARE THE SYMPTOMS OF POISON IVY AND POISON OAK?
Almost everyone who has ever gotten poison ivy or poison oak can tell a doctor that their symptoms are itching, itching, and more itching. Frequently, the symptoms start out as very mild itching on a finger, hand, or forehead. You may not even see anything. You just start scratching or rubbing the skin. After a few hours or even a day, you notice that the skin where you have been rubbing and scratching is red and some small bumps are appearing. You also notice that several parts of the body seem to have the same thing happening.
The bumps of poison ivy and poison oak are usually small and red. At first, the bumps may appear isolated to different places of the body. Then they seem to come together into larger areas, often following “lines”, as if someone took a feather and drew it across the skin. This is in fact what has happened, as the leaf of the plant has drawn across the skin.
In fact, wherever the plant touched the skin, the rash will break out. Your skin, however, reacts at different times. This is important to know, because most people think that their poison ivy and oak are “spreading,” when in fact it is not. So, what may appear to you as spreading poison ivy is simply your skin reacting to the chemical poison at different times. The effect, however, is that you often cannot tell the full extent of poison ivy or poison oak simply by looking at what it looks like early on in the disease, in the first day or two. It will usually get worse. This is a really important piece of information to know, because your symptoms will also usually get worse.
As the condition gets worse, the small bumps come together and form groups of bumps called vesicles. These vesicles contain clear or honey-colored fluid with all kinds of cells that are reacting to the irritated skin. As you scratch more and more, the bumps and vesicles get more irritated and break open, forming crusts on the skin.
Often, people keep scratching these vesicles until they bleed. The reason is that the sensation of pain is less bothersome to most people than the symptoms of itching. Unfortunately, if you scratch your rash until it bleeds, it also means that you stand a chance of your rash getting infected with bacteria. In this case, you may need to take oral antibiotics. (See section on treatment below.)
HOW LONG WILL THE RASH LAST IF I DO NOTHING?
Most cases of poison ivy and poison oak will go away on their own within two or at most three weeks (See figure below). Some cases can last as long as a month. Many people do not recognize what the plant looks like, so they get repeated exposure and repeated outbreaks, particularly during the summer months.
HOW DO I KNOW IF I HAVE POISON IVY OR POISON OAK?
If you start itching in the summer, on several parts of your body, particularly your hands or arms or face, and then develop small red bumps that start to appear in streaky lines, with lots and lots of itching, then you may have poison ivy or poison oak, particularly if you were working or walking outdoors in the woods 1-2 days previously.
Many other diseases can look like poison ivy or poison oak initially, so it is not always easy to tell the difference, particularly early on in the process. Eczema (shownbelow) is a disease of dry skin that can cause itching over much of the body, but it is usually chronic and not acute. If poison ivy or poison oak occurs in someone who also has eczema, the skin irritation can be very great.
Poison ivy and poison oak can also look similar to some skin reactions to drugs. Allergies to other plants or even things like clothes, detergents, or latex, can have a similar appearance. Usually, allergies to most other items are symmetrical, that is, the rash looks fairly even on both sides of the body. In contrast, the rash of poison ivy and poison oak is usually not symmetrical, reflecting the rather chance locations that the plant has encountered the skin.
Finally, a disease called scabies, caused by a parasite, can also cause very severe itching of the skin, but it does not usually have vesicles that ooze fluid, and the distribution of scabies is often confined to the wrists, finger webs, underarms, waste, groin, ankles and toe webs.
IS POISON IVY OR POISON OAK CONTAGIOUS?
As mentioned earlier, you cannot get poison ivy from someone who has it, only from the exposure to the plant itself. Thus, if you touch someone else’s’ rash, you should not get the disease. Of course, why would you touch someone else’s rash, as it is their rash, not yours!
WILL I SPREAD POISON IVY ON MY BODY BY SCRATCHING IT?
The answer, as described above is no, no, and no. It may appear that way to you, but that is actually just where the plant originally touched your skin, and the skin reacts differently and at different times.
HOW DO I TREAT POISON IVY AND POISON OAK?
If you have poison ivy or poison oak limited to a small area, you can sometimes treat it by using creams that you can buy in your local drug store.
If the rash occurs on more than one arm and leg, if it occurs on your face, or if it causes you to scratch at all hours of the day or night, you probably want to talk to your doctor about getting a prescription medication called corticosteroids. You can get this medication as either a topical preparation to apply to your skin or pills you take by mouth.
Topical steroids prescribed by physicians come in many strengths, and you usually only need to apply them once or twice a day. They help but often times do not fully remove the itching, and once the full blown rash comes out, they are less effective.
For severe itching or disease that involves many parts of the body, doctors usually recommend oral corticosteroids, usually called prednisone. Prednisone is usually given at higher doses for the first several days and then the dose is lowered over 7-14 days. It is very important to take the prednisone pills exactly as your doctor directs. If you stop the prednisone too soon, the rash of poison ivy and poison oak will likely come back. Prednisone is highly effective in treating the rash and itching, and it can be taken usually only once a day.
Many over-the-counter lotions, creams, and ointments can help with itching. Some of these (Hytone, Cortaid, Cortisone, Aquanil HC, Dermtex) contain 0.5-1% hydrocortisone cream, a mild anti-inflammatory medication. Products that contain Calamine are soothing to the skin, and as they evaporate, the itch temporarily improves. Some products contain phenol, menthol, camphor or pramoxine that can ease itching temporarily. Brand names of these products include: Gold-Bond anti-itch cream, Tecnu rash relief spray, Calagel anti-itch gel, Pramoxine Anti-itch lotion, Dermoplast spray, Pramegel, Prax cream and lotion, Itch-X spray and gel, and Sarna cream and foam. Oatmeal baths, such as Aveeno, can also provide temporary relief.
Sometimes, an oral antihistamine (allergy pill), such as diphenhydramine, can also help lessen the itching. Topical antihistamines should be avoided however, as they can make the skin even more sensitive. You should ask your doctor about all these medications.
One of the best things you can do to ease the itching is put cold compresses on the rash. To do this, put a clean cloth in cool water, and then wring out the excess water. Burow’s solution is a medication (aluminum acetate) added to cool compresses that has a cooling and drying effect to decrease itching. One of the worst things you can do for the itching is to put heat on it, as this will simply cause it to become more irritated and itch more. You may notice that the itching worsens, for example, after you take a hot shower.
HOW CAN I AVOID GETTING POISON IVY OR OAK?
The best way to not get poison ivy and poison oak is to recognize the plant and avoid touching it if at all possible. The plants have a usual appearance as three-leaved groupings arising from a central red stem. Posion oak resembles leaves of an oak tree. The leaves of poison ivy are frequently quite shiny. An old rhyme is useful to remember: “Leaves of three, let it be”. Even when dried, the leaves can cause a rash if you touch them or the stem, so cutting down old poison ivy vines in the winter can still be problematic. If the leaves touch your pants, clothes, or gloves, make sure you wash the clothes or gloves thoroughly before wearing them again.
When hiking or gardening in areas with poison ivy, it is important to wear protective pants, long-sleeve shirt and even gloves. Do not burn poison ivy plants, as the fumes can cause a severe allergic reaction to those with sensitivity to the plant poison. Also, if you are hiking with a pet in an area with poison ivy, make sure you wash the pet after hiking to prevent the pet giving you the disease from exposure to the urushiol on the pet’s fur.
Some people who garden frequently in areas with lots of poison ivy may choose to use a product called IvyBlock, a lotion that contains Bentoquatam. This lotion may bind to urushiol and thus block the ability of urushiol to attach to the skin. It must be used at least 15 minutes before exposure to the plants, and it should not be used by children younger than seven years of age. It also must be reapplied after being exposed to the plants for more than four hours, and it leaves a clay-like residue on the skin after it dries.
Some people also consider using barrier creams that are about 60% effective in preventing poison ivy when applied liberally to the skin before being exposed. A study in 1992 from Duke University showed that products such as StokoGard barrier cream, Hollister Moisture Barrier cream or ointment, and Hydropel ointment are effective.
WHAT SHOULD I DO IF I TOUCH THE POISON IVY OR POISON OAK PLANT?
If you know that you have touched the plant and did not have gloves on, the very first thing you should do is immediately wash your hands with soap and water, or even wipe them down with rubbing alcohol followed by water. If you can do so within 5-10 minutes of exposure to the plant, you may be able to avoid getting the reaction. After 30 minutes, washing the skin is good, but you will likely still get the skin reaction and disease.
You can use several mild, over the counter detergent creams to cut down on the reaction you might get if you were not able to wash the skin in the first thirty minutes but you had significant exposure to poison ivy. One chemical that can decrease the reaction up to several hours after exposure is called Tecnu skin cleanser. You apply this cream for two minutes to places where you were exposed to the poison ivy or poison oak plant, and then wash with water. Goop hand cleaner in a gel, liquid or soap is another product designed to remove the oil resin from the skin. Finally, you can purchase a soap mixture of that combines ethoxlate and sodium lauroyl sarcosinate surfactants, called Zanfel, that can help remove urushiol in contact with the skin.
SHOULD I PUT BLEACH ON THE RASH?
Absolutely not! Using bleach on the skin is like putting a second poison on the skin. You will kill off several layers of skin, and your skin may hurt more than it itches for a while. Subsequently, you risk making the skin reaction much worse, including having infections of the skin.
CAN MY CHILD GO TO SCHOOL OR CAMP IF THEY HAVE POISON IVY OR POISON OAK?
Absolutely! Since poison ivy and poison oak are not contagious to others, no reason exists to keep children away from other children. Do not think, however, that teachers, school administrators or even other children will know all the information that you now know. You may need to educate them about the disease, or even get a doctor’s note saying that everything is okay.
WHAT ELSE DO I NEED TO KNOW?
If your rash does not get better, or if it worsens, you should see your doctor. It is also important to see your doctor if you develop a fever, if the rash covers a large area of your body, or if there is pus coming from the bumps on your skin. These symptoms may indicate that you need more than just over-the-counter treatments.
As mentioned above, sometimes other things can cause a severe itching rash, such as allergies to other substances. Your doctor can help determine what is causing the condition, and they will offer the best treatments available.
Source:
http://knol.google.com/k/poison-ivy-and-poison-oak#
http://knol.google.com/k/poison-ivy-and-poison-oak#
Tuesday, November 22, 2011
Knee Surgery - A Guide for Patients and Healthcare Professionals
Author:
Justin D. Harris, MD
Orthopaedic Surgeon
Lincoln, NE
This knol provides a general overview of sports-related knee injuries. It is intended to provide basic information for patients and other healthcare professionals regarding the most commonly treated knee conditions.
Mechanism of injury, symptomatology, treatment options, and basic rehabilitation principles are discussed for each condition.
Introduction
Knee injuries and knee pain are extremely common. Knee problems are the most common reason patients need to see an orthopaedic surgeon. The knee is an extremely complex joint that is subjected to large forces during daily and athletic activities. Sports injuries frequently involve the knee, and as we age, degenerative knee problems develop. Many knee injuries can be treated conservatively (without surgery), but certain knee conditions benefit from surgical intervention.
Anatomy and Function
The knee is the largest joint in the body. Knee function primarily involves bending (flexion) and straightening (extending) the leg. Rotation also occurs within the knee. Anatomically, it is composed of the lower end of the thigh bone (distal femur) and upper end of the shin bone (proximal tibia). The front of the knee is covered by the knee cap (patella) that slides in a groove in the distal femur (trochlea) during knee motion.
The ends of the femur and the tibia, as well as the undersurface of the patella, are covered with cartilage. This cartilage has been described as the “white on the end of a chicken bone.” This “articular cartilage” serves to help with joint motion by providing lubrication and minimizing friction. Deterioration or wear of this articular cartilage is termed arthritis.
The knee also contains two “shock-absorber” pieces of cartilage called menisci. The medial meniscus sits between the femur and the tibia on the inner part of the knee, whereas the lateral meniscus occupies the outer part of the joint. Meniscal function is to provide cushion for the bones of the knee.
Knee stability is provided the ligaments of the knee. The cruciate ligaments (ACL and PCL) are in the center of the knee and serve to resist translational and rotational moments about the knee. The medial collateral ligament (MCL) is on the inner part of the knee connecting the femur and the tibia. The lateral collateral ligament (LCL) is on the outer part of the knee. The collateral ligaments resist side-to-side movements about the knee.
Lastly, the quadriceps tendon and the patellar tendon make up the extensor mechanism of the knee. The quadriceps are the muscles on the front of the thigh. At the knee, they form a tendon that inserts on the knee cap. There is a second tendon that runs from the knee cap to the top of the tibia (shin bone). These tendons as well as the patella allow us to straighten the knee from a bent position.
www.aclsolutions.com
http://www.leadingmd.com/patientEd/meniscus/overview.asp
Orthopaedic Knee Evaluation
The orthopaedic knee evaluation typically involves a detailed medical history, a thorough knee examination, and imaging studies. The medical history involves questions about the patient’s health as well as details regarding their knee symptoms. Important factors to consider are the duration and intensity of symptoms. The location and quality of the pain are also important. Knee conditions may often involve swelling, mechanical symptoms (popping, catching, locking), and sensations of instability. Alleviating and aggravating factors are important to mention.
The knee evaluation involves checking the back and the hip to ensure that the pain is coming from the knee. Inspection of the muscles and the alignment of the leg is next. Range of motion and walking observation follow. The surgeon will then palpate specific areas of tenderness to try to determine the location of the pathology. Lastly, specific tests are performed to assess the quality of various tissues in and about the knee (menisci and ligaments).
Most surgeons will order x-rays to look at the bony structures of the knee. Fractures, leg malalignment, and arthritis will often be noted on x-rays. Soft tissue structures (cartilage, menisci, and ligaments) are best evaluated with an MRI.
After compiling all the information from the history, physical examination, and imaging studies, the orthopaedic surgeon will make a diagnosis and present
a treatment plan. Treatment options may include medications, physical therapy, or orthotics. Surgery may be recommended. The surgeon will then describe the surgical procedure, explain the risks and benefits associated with the procedure, and detail the expected postoperative recovery.
Knee Surgery
Various injuries and conditions within the knee are treated operatively. Indications for surgical treatment vary, based on individual diagnosis. Certain conditions may fail to respond to conservative management, whereas other injuries are treated more aggressively. The goal of all treatment is to try to return the patient to their previous level of activity and function.
Knee surgery can be performed arthroscopically or in an open fashion. Arthroscopic surgery allows an orthopaedic surgeon to diagnose and treat knee injuries by viewing the inside of the knee through small incisions using a pencil-sized instrument called an arthroscope. The knee is filled with fluid and the scope transmits an image of the knee through a camera to a television monitor. During the procedure, additional small incisions are created to allow insertion of other small instruments to remove or repair damaged tissues. Most arthroscopic knee procedures are done as an outpatient. Recovery is typically much quicker and easier than traditional open knee procedures.
Open knee surgery involves larger incisions to enter the knee joint (arthrotomy).
These operations are more extensive and often more complex than most arthroscopic procedures. They may be done as an outpatient, but a short inpatient stay afterward is not uncommon.
Rehabilitation for knee injuries and after knee surgery varies based on the patient’s specific injury complex and the surgical procedure that was performed. Physical therapy can be utilized as a nonoperative modality for a number of knee conditions. The primary goals of PT for knee pain include maximizing range of motion, improving flexibility, and strengthening the muscles around the knee to take stress off of injured tissues.
Postoperative rehab can be quite variable. Some simple knee surgeries don’t require formal therapy at all, whereas other procedures require months of dedicated physical therapy to achieve maximum results.
A more detailed description of individual surgical procedures and the expected postoperative recovery follows.
Meniscal Injuries
Meniscal injuries are the most commonly surgically-treated knee condition. The menisci are shock-absorber cartilage between the femur and the tibia. The medial meniscus is on the inner portion of the knee, whereas the lateral meniscus is on the outer part of the knee. Young patients typically sustain meniscal injuries during athletic activities. Cutting and pivoting can stress the meniscus to the point that it tears. Older patients tear their menisci during less vigorous activities. As we age, the meniscus starts to degenerate and can tear with trivial trauma. A large percentage of older patients actually have asymptomatic meniscal tears.
Symptoms of a torn meniscus include recurrent swelling (effusions), mechanical symptoms (popping, catching, and locking), and pain with deep squatting. The pain is typically localized to one side of the knee or the other. A medial meniscus tear hurts on the inside of the knee, while a lateral meniscal tear hurts on the outside. Cutting, pivoting, and athletic activities may be difficult with a meniscus tear.
Surgery for a torn meniscus is typically done arthroscopically. The specific surgical procedure that is performed is dependent on a number of factors. It is important to try to preserve meniscal tissue because arthritis tends to develop faster in knees that have less meniscus remaining.
Meniscus tears that occur in young patients and are located near the edge of the meniscus (best blood supply) are often repairable. Meniscus tears near the central surface and those that occur in older patients are often removed (partial meniscectomy) because they lack the capacity to heal. In some select situations, patients that have had a significant portion of their meniscus removed may be a candidate for a meniscal transplant, where a cadaver meniscus is placed in the knee to try to prevent joint degeneration.
Partial Meniscectomy
Arthroscopic partial meniscectomy is the most common arthroscopic procedure that surgeons perform. Patients that have symptomatic meniscal tears are usually good candidates for arthroscopic surgery. If a surgeon determines that a meniscal tear is unlikely to heal, the torn meniscal tissue is removed surgically. This is called a partial meniscectomy. (Fi
Partial meniscectomies are performed arthroscopically. Once the torn tissue has been removed from the knee, patients typically feel much improved. The postoperative course is fairly straightforward. Most patients are on crutches for a couple of days to help stabilize the knee. Once the swelling subsides, the rehabilitation progresses quickly. Most patients can return to work after only a few days. Return to sports is permitted once the swelling is gone, and the patient has normal quadriceps function.
Video of a partial medial meniscectomy
More video of a partial medial meniscectomy
Meniscal Repair
Meniscus repairs are typically reserved for younger patients (< 40 years of age) who have a tear that is located near the outer rim of the meniscus. The goal of all meniscal surgery is to preserve meniscal tissue, but repairs are only indicated where healing can be expected.
Surgeons employ various meniscal repair techniques. The basic principles involve placing suture or some type of bioabsorbable implant across the tear, which will stabilize it until it heals. Smaller tears are amenable to repairs with meniscal fixation devices placed arthroscopically (all-inside). Larger tears occasionally require a secondary incision on the side of the knee (inside-out). Results of successful healing after meniscal repair vary from 60%-80%.
The postoperative rehabilitation following a meniscal repair will vary based on surgeon preference, but basic guidelines are usually followed. The meniscus typically takes a few months to be fully healed so the repair must be protected during that time. Most patients are placed in a hinged-knee brace at the time of surgery. They can bear weight within the brace but usually only locked in full extension (leg straight). Range-of-motion exercises are allowed but higher degrees of flexion are usually avoided (< 90).
After the first month the brace is unlocked during weight bearing, and higher knee flexion is permissible. Most patients are allowed to return to sports anywhere from 3 to 6 months after surgery, depending on the severity of the tear.
Ligament Injuries
There are four main ligaments around the knee. The ACL, PCL, MCL, and LCL have been described previously. Injuries to these structures are not uncommon. As we have become a more active and a more sports-oriented society, the incidence of knee ligament injuries has increased. Treatment of knee ligament injuries is based on multiple factors. Each individual ligament is treated differently. Patient age, health, and activity level all play a role in determining optimal treatment. Additional pathology within the knee can also alter the treatment plan.
Anterior Cruciate Ligament Injuries
ACL injuries occur through some form of twisting mechanism. This can occur while the foot is planted on the ground or after landing awkwardly from a jump. Additionally, a “contact” injury can occur where the knee is forced in an abnormal position by an outside stress.
Acute symptoms of an ACL injury include hearing or feeling “a pop.” Swelling of the knee can develop quite quickly. In chronic settings, knee instability becomes more common, especially during cutting and pivoting activities.
The treatment of ACL injuries is dictated by the patient’s activity level and expectations. Patients who live a sedentary lifestyle may not need to have their ACL tear treated surgically. However, athletes who wish to regain the ability to participate in cutting and pivoting sports will likely benefit from ACL surgery.
Anterior Cruciate Ligament Reconstruction
Anterior cruciate ligament tears usually cannot be repaired. As such, a reconstruction or “ACL replacement” must be performed. The most common type of ACL reconstruction involves taking tissue and creating a new ligament which is then placed within the knee. This serves to replace the torn ACL.
The most concerning issue for patients undergoing ACL reconstruction is the graft source. The new ACL can come from the patient (autograft) or it can come from a cadaver (allograft). There are risks and benefits to both options. The most common autograft options are patellar tendon and hamstrings.
ACL reconstruction is typically done as an outpatient procedure. Depending on graft choice, open incisions may be necessary to harvest the tissue that is to be used as the new ACL. Knee arthroscopy is then performed to inspect the knee, treat additional injuries (meniscus tears or cartilage damage), and to prepare the knee for the new ACL.
Once the graft tissue has been prepared and the torn ACL tissue has been removed, the surgeon is ready to place the ligament within the knee. Small tunnels (7-10 mm) are drilled in the tibia and the femur to allow the ligament to be pulled up into the knee.
Accurate placement of these tunnels is critical to successful ACL surgery. After the ACL graft is in position, fixation devices (screws, washers, buttons, etc.) are used to keep it there until it can heal into place.
Rehabilitation after ACL reconstruction is a necessary part of a successful procedure. The patient is placed in a brace after surgery. Therapy is started shortly thereafter. Weight bearing is typically allowed immediately. Maintaining full extension and minimizing swelling are early goals. Range of motion activities then begin. Strengthening of the leg comes next, with gradual return to straight ahead running. Sport specific rehab and cutting and pivoting are the last steps prior to return to athletics. The typical athlete is held out of sports for 6 months following ACL reconstruction.
Posterior Cruciate Ligament Injuries
Posterior cruciate ligament (PCL) injuries are much less common than ACL tears. The most common mechanism of injury involves a direct blow to the front of the tibia. This can occur during sports or in motor vehicle collisions. The tibia is forced backwards relative to the femur and the PCL tears. Other common athletic mechanisms include knee hyperextension and forced knee flexion with the foot plantar flexed. Acutely, PCL tears can present similarly to other knee injuries. Swelling, pain, and instability are common. In the chronic setting, persistent instability may occur.
Management of isolated PCL tears is typically conservative. Once the acute swelling and discomfort of the initial trauma subsides, physical therapy is utilized to try and maximize quadriceps strength to assist with dynamic knee stability. After completion of a dedicated rehab program, the patient is allowed to return to play once full motion and near-normal strength have returned.
Posterior Cruciate Ligament Reconstruction
PCL surgery is much less common than ACL surgery. Surgical intervention is typically reserved for specific indications. PCL tears that pull a piece of bone off of the tibia (avulsion fracture) may benefit from operative fixation. PCL injuries that occur in conjunction with other knee ligament tears (knee dislocations) often benefit from surgical reconstruction. Finally, patients who have had PCL tears treated conservatively, but still complain of instability are candidates for PCL reconstruction.
PCL reconstruction involves taking tissue from another source and creating a new PCL. Autograft or allograft sources can be used to make the PCL graft. Graft choice is determined after a discussion of risks and benefits of each option between the patient and the treating orthopaedic surgeon. Isolated PCL reconstruction can often be done as an outpatient procedure, whereas multiple ligament knee surgery typically requires a short hospital stay. PCL surgery is usually done as an arthroscopic procedure, although some small open incisions are often required. An added degree of difficulty exists when compared with ACL reconstruction, because the PCL attachment site on the tibia can be more challenging to access. Just as in ACL reconstruction, the torn PCL is removed arthroscopically. Tunnels are then drilled in the tibia and the femur to allow passage of the PCL graft. The new PCL is then pulled into the knee and fixed to the bone.
Rehabilitation after PCL reconstruction varies based on surgeon preference. Braces are typically worn in the early postoperative period. Weight bearing may be delayed in some instances. Postoperative therapy focuses on quadriceps strengthening to prevent the tibia from sagging backward, which can stretch the PCL graft. Most patients return to sports and full activity 6-8 months after surgery
Medial Collateral Ligament Injuries
Medial collateral ligament (MCL) injuries occur when the knee buckles to the inside. This often happens when an athlete sustains a direct blow to the outside of the knee forcing it inward. Pain is felt on the inner (medial) part of the knee. Noncontact injuries often result in isolated partial MCL tears, whereas contact mechanisms can produce complete MCL tears and may injure other knee ligaments as well (ACL).
The most common symptom following a medial collateral ligament injury is pain directly over the ligament. Swelling over the torn ligament may appear, and bruising and generalized joint swelling are common 1 to 2 days after the injury. In more severe injuries, patients may complain that the knee is unstable, or feel as though their knee may “give out” or buckle.
The majority of MCL injuries are treated conservatively (without surgery). The duration of convalescence is dependent on the severity of the injury. Partial MCL tears usually heal quickly and athletes return to play within a couple of weeks. Minimizing swelling and maintaining range of motion are essential to facilitate a quick recovery. Complete MCL tears may take more than 6 weeks to heal. Pain, swelling, and stiffness are common. Bracing is usually utilized to help the ligament heal under normal tension. Range of motion exercises are emphasized during rehab to prevent knee stiffness from developing. Complete rehab from a full thickness MCL tear can take 3-4 months in some situations.
http://www.kneeguru.co.uk/html/steps/step_03_collaterals/injury.html
Medial Collateral Ligament Repair/Reconstruction
As stated previously, most MCL injuries don’t require surgery. However, certain surgical indications do exist. High-grade (complete) MCL tears that coexist with other knee ligament injuries may benefit from surgical repair. Additionally, MCL tears that have healed with residual laxity (looseness), causing persistent instability of the knee, often benefit from repair or reconstruction.
MCL surgery is done via an open incision on the inner portion of the knee. If the operation is done in the acute setting (< 3 weeks after injury), primary repair of the torn ligament is possible. Midsubstance ruptures are reapproximated (connected) and sutured together with large caliber permanent suture material. Tears that pull of off the ligament’s bony attachment sites are usually put back down to the bone with suture anchors.
In cases of chronic MCL laxity and instability, MCL reconstruction is often necessary. In these instances, a new MCL is fashioned from autograft or allograft tissue. The new ligament is then placed over the top of the old MCL and secured to the femur and the tibia with fixation devices.
Rehabilitation after MCL surgery is similar to that of other knee ligament postoperative protocols. The knee is protected in a brace for a few weeks after surgery. Range of motion exercises are initiated early to prevent stiffness. Strengthening begins 6-8 weeks after surgery. Complete rehab takes 4-6 months.
Lateral Collateral Ligament/Posterolateral Corner Injuries
Lateral collateral ligament (LCL) injuries occur when the knee buckles outward. These are typically high-energy contact injuries where a force is applied to the inner part of the knee which then stretches or tears the ligament on the outside. Pain is felt on the outer part of the knee over the LCL. Symptoms are similar to other knee ligament injuries.
Isolated LCL injuries do well with conservative management. Rest, icing, and early motion permit a relatively quick return to sports and activity. Unfortunately, injuries to the lateral side of the knee often produce more trauma than just isolated LCL tears. The posterolateral corner (PLC) is a complex of ligamentous structures behind the LCL that serve to resist varus (outward) stress, posterior (backward) displacement of the tibia, as well as external rotation of the knee. PLC injuries typically occur in conjunction with other knee ligament injuries. They are often misdiagnosed and can play a role in why other ligament surgery (ACL/PCL) fails.
Lateral Collateral Ligament/Posterolateral Corner Repair/Reconstruction
Surgery for the LCL/PLC is typically reserved for knees with multiple ligaments that are injured. Common combinations include ACL/PLC injuries and PCL/PLC injuries. Knee dislocations often have PLC involvement as well. In most settings, if the LCL/PLC is ignored, the results of cruciate reconstruction will be diminished. Lateral-sided knee injuries are repaired through open incisions. For acute injuries, primary repair of the PLC is possible. The tendons and ligaments that are injured are sutured together primarily or are reattached back to their insertion points on the bony structures. In the chronic setting, the LCL and PLC have healed and scarred together with residual laxity. Primary repair is not possible. As such, reconstruction is then performed with autograft or allograft tissue. Multiple reconstruction techniques have been described. Postoperative management is similar to that described above.
Articular Cartilage Injuries
Articular cartilage is the smooth, glistening, white tissue that covers the ends of bones in the human body. It functions to resist compressive loads in joints and provides a smooth surface with low friction to allow for supple joint movement. Injury to articular cartilage is extremely common. Traumatic events can damage cartilage, and as we age, the biology of the cartilage changes, predisposing it to wear and injury. Cartilage injuries are concerning because articular cartilage lacks a blood supply, which prevents it from healing.
Articular cartilage injuries can occur as a result of either traumatic mechanical destruction, or progressive mechanical degeneration (wear & tear). ACL tears, patellar dislocations, and other knee injuries can present with acute articular cartilage damage. Typically, these mechanisms of injury create small, focal defects in the cartilage. Degenerative cartilage lesions can be shallower but often involve more overall surface area. Additionally, osteochondritis dissecans (OCD) is a condition where the bone behind the articular cartilage is diseased, which may lead to a large defect if a piece of cartilage were to detach from the underlying bone.
Symptoms of articular cartilage damage include knee swelling and vague pain. Mechanical symptoms (catching and locking) may also be present. With mechanical degeneration (wear and tear), the patient often experiences stiffness, decreased range of motion, joint pain and/or swelling.
Cartilage injury is difficult to diagnose by history and physical exam alone. Radiographs (x-rays) and an MRI of the knee are helpful to evaluate the health of the cartilage. X-rays are used to look for moderate to severe signs of arthritis (diffuse cartilage degeneration). MRI is helpful to look for focal cartilage lesions as well as to look for loose bodies (pieces of cartilage that have detached and are floating in the knee) and additional pathology within the knee.
Treatment of articular cartilage lesions is dependent on multiple factors. Patient age, activity level, and mechanism of injury commonly dictate management. Young patients with traumatic injuries are treated aggressively to try to restore a normal articular surface within the knee. Older patients with degenerative cartilage problems can initially be treated conservatively.
Nonoperative treatment is indicated for patients who present with diffuse osteoarthritis. Management consists of physical therapy, medications activity modification, orthotics, bracing, and injections. Failure of conservative management may be an indication for surgical intervention, depending on the patient’s symptomatology.
Operative management for cartilage injuries is reserved for acute traumatic defects, OCD lesions that are deemed to be unstable (at risk for detachment), and loose bodies within the knee. Small focal lesions can be treated conservatively, but this is usually unsuccessful. Large lesions should be treated aggressively to prevent joint deterioration. The specific surgical procedure to treat articular cartilage lesions is dictated by the lesion size, the quality of the bone behind the lesion, and surgeon preference.
Loose Body Removal
Loose bodies within the knee often cause symptoms of pain, catching, and locking. Symptomatic loose bodies should be removed. This is performed as an outpatient, arthroscopic procedure. The surgeon uses the arthroscope to find and localize the loose bodies and they are removed with an arthroscopic grasper. The remainder of the knee is evaluated and any additional pathology is treated appropriately.
Rehab after simple loose body removal is fairly straightforward. Crutches may be needed for a couple of days, but patients are allowed to return to full activity once swelling and range of motion have normalized.
Arthroscopic Chondroplasty
Arthroscopic chondroplasty is commonly performed during knee arthroscopy. It is utilized for treating incidentally-found chondral lesions during surgery. It can also be utilized for small areas of superficial cartilage damage in patients that experience joint pain and have associated mechanical symptoms. Loose cartilage flaps and debris within the knee are removed using an arthroscopic shaver. Great care is taken to avoid damaging normal cartilage. The goal of surgery is to eliminate catching and locking from these loose pieces of cartilage and to try to prevent propagation of these chondral flaps. The postoperative management is identical to that of basic knee arthroscopic procedures described previously.
Microfracture
Small, focal lesions (< 2 cm) of cartilage damage that are surrounded by healthy tissue are often treated with a microfracture procedure. As cartilage has no blood supply, it lacks the ability to heal. The bone beneath the cartilage, however, has a rich blood supply. Microfracture procedures try to access the osseous vascular supply in order to heal cartilage defects. Microfracture creates small holes in the bone at the base of a cartilage lesion. This allows cells from the bone marrow to fill in the defect and stimulate new cartilage growth. This new cartilage is a scar-type of cartilage called fibrocartilage. It is less durable than normal hyaline cartilage, but provides a smooth covering of the lesion.
Indications for microfracture are small to moderately-sized focal cartilage lesions. Widespread cartilage damage is a contraindication to a microfracture procedure. It is done arthroscopically. The cartilage defect is evaluated and measured by the surgeon. Loose cartilage flaps are removed with a shaver. Then, a small, sharp pick (awl) is used to create the small microfracture holes in the bone. The number of microfracture holes created depends on the size of the area being treated. Most patients with a 1- to 2-centimeter area of damage require 5 to 15 small holes in the bone.
The postoperative management of a microfracture procedure is critical. Surgery is typically done as an outpatient. The patient is kept non-weight bearing and on crutches for 6-8 weeks following surgery. Range of motion is essential after surgery to allow the fibrocartilage to grow and mature into a normal shape. Many surgeons will use a CPM (continuous passive motion) machine after surgery to facilitate this. Microfracture done in the area of the kneecap (patellofemoral joint) is rehabilitated somewhat differently, in that motion is restricted to avoid excess pressure placed on the healing area.
Autologous Chondrocyte Implantation
Another option for attempting to heal cartilage lesions is autologous chondrocyte implantation (ACI). This procedure is reserved for patients with small to moderate-sized lesions who have usually failed a previous procedure (chondroplasty or microfracture). The procedure is complex, and the rehab is extensive so appropriate patient selection is critical. It is a two-stage operation in which cartilage cells are harvested from the knee, grown in a lab, and then reimplanted into the knee during a second operation.
The first step of an ACI surgery is to perform an arthroscopic procedure where the cartilage defect is evaluated. If the lesion is appropriate for ACI (based on size, depth, and quality of the surrounding cartilage), small pieces of normal cartilage are harvested from less essential areas of the knee. This cartilage is then sent to a cartilage expansion laboratory where the cells are cultured and multiplied. Once enough cells have been grown, the second stage of the operation is scheduled.
The second stage of ACI surgery involves implantation of the cartilage cells. This is done as an open procedure. The area of cartilage damage is exposed and sized. A second incision is then made over the shin and a “patch” is harvested from the thick tissue (periosteum) that covers the shin bone. This patch is roughly the size of the cartilage lesion being treated. The patch is then sewn over the cartilage defect and the cultured cells are injected underneath the periosteal patch.
The rehab after ACI is similar to that of microfracture. Weight-bearing is restricted and crutches are required for 6-8 weeks while the cells adhere to the underlying bone. Motion is encouraged, often with the use of a CPM. Training intensity increases from 3-6 months postoperatively, but most athletes don’t return to sports for 12-16 months following surgery.
Osteochondral Autograft Transfer
Another surgical option for symptomatic, focal articular cartilage lesions is an osteochondral autograft transfer. This is also referred to as a mosaicplasty, or an OATS procedure. Mosaicplasty involves harvesting normal cartilage from the knee and transferring it to replace the area of damaged cartilage.
Indications for mosaicplasty are similar to that of ACI. Lesions < 2 cm in diameter are ideal. This is not a procedure utilized to treat diffuse cartilage damage. The surgery can be done arthroscopically or open. It is commonly performed as an outpatient. The cartilage defect is usually evaluated and prepared arthroscopically. If the lesion is appropriate for mosaicplasty, appropriately-sized osteochondral plugs are harvested from another part of the knee joint. The cartilage in this “donor area” is not as essential because it is subjected to less pressure during weight-bearing. The plugs are then transferred to the cartilage defect and set into place.
The rehab after osteochondral autograft transfer is similar to that described previously. Weight bearing is restricted for 6-8 weeks. Motion is encouraged. Return to sports and full activity is permitted after 6 months of rehab in most cases.
Osteochondral Allograft Transplantation
Large, focal cartilage lesions (> 2 cm in diameter) are often too large to be treated with microfracture, ACI, or mosaicplasty. For these patients, an allograft is often the only tissue source large enough to provide enough cartilage to cover the defect. An allograft is donated tissue that comes from a cadaver. Patients who are candidates for allograft transplantation have their imaging studies (x-rays or MRI) sent to a tissue bank which tries to procure a graft that is size matched to the patient. When a graft is found, surgery is scheduled.
Osteochondral allograft transplantation is typically done as an open procedure. A short hospital stay is not uncommon. The area of damaged cartilage is prepared by coring a socket 4-5 mm deep into the subchondral bone. The exact same location is then identified on the allograft specimen and a plug is created that fits perfectly into the host femur. The allograft plug is then placed within the recipient socket. The goal is to create a flush, smooth surface of articular cartilage.
The postoperative management of osteochondral allograft transplantation is slower than that of other cartilage restoration procedures. The bony portion of the graft needs to be replaced by bone from the patient, and while this occurs the graft is susceptible to collapse. As a result, weight-bearing is restricted for 10-12 weeks. Motion is encouraged early. Patients are allowed to return to full activity 12 months after surgery.
Patellofemoral Disorders
The patellofemoral joint is the articulation between the undersurface of the kneecap (patella) and the groove in the front of the femur (trochlea). It is a common source of pain and disability in patients. Patellofemoral issues commonly present as pain in the front of the knee (anterior knee pain). Aggravating factors include stair climbing and standing up from a seated position. Multiple conditions can present with patellofemoral pain, which can make determining optimum treatment difficult. Fortunately, most anterior knee pain responds to conservative management, but specific surgical indications do exist for some conditions. More detailed descriptions of these conditions follow.
Lateral Patellar Compression Syndrome
Lateral patellar compression syndrome (LPCS) is a common condition that presents with anterior knee pain. It is characterized by a tight lateral retinaculum (tissue on the outside of the patella). This tight tissue causes abnormal motion of the patella within the trochlea. This can be exacerbated by other patient factors, such as limb alignment and muscle strength. Patients with LPCS have limited medial (inside) mobility of the patella and may have a patella with excessive lateral tilt.
Conservative management is indicated in all cases of LPCS. Physical therapy is the mainstay of treatment. Quadriceps strengthening, flexibility training, and patellar taping all can be beneficial. A patellar sleeve or brace can also be helpful during athletic activities. A dedicated course of nonoperative treatment needs to be attempted before considering surgical intervention for LPCS.
Lateral Release
The most common surgical intervention for LPCS is a lateral release. This procedure involves surgically dividing the tight lateral retinaculum that is tethering the patella. It is most often done arthroscopically as an outpatient procedure. There is a mild risk of excessive bleeding within the knee after the release. Results for this procedure are good if strict surgical indications are followed. The rehab postoperatively involves minimizing swelling initially, followed by dedicated quadriceps strengthening.
Patellar Instability
Patellar instability occurs when the kneecap slides out of its groove (trochlea) as the knee bends. Most commonly, the patella displaces (dislocates) in a lateral direction (toward the outside). Patellar instability can be described as acute or chronic. Acute patellar dislocations occur when a twisting force is applied to the lower leg. The femur rotates inward while the tibia and the patella rotate outward. This can result in a patellar dislocation.
Chronic patellar instability occurs in patients that have developed specific anatomic risk factors. A wide pelvis, a shallow trochlea, a high-riding patella, knock-knees, flat feet, and underdeveloped thigh musculature are all risk factors for recurrent patellar instability.
The treatment of acute patellar dislocations is typically nonsurgical. A brief period of immobilization (4 weeks) is followed by a dedicated rehabilitation program. Rehab should focus on quadriceps strengthening exercises and flexibility training. The primary surgical indication for an acute patellar dislocation is when a piece of cartilage breaks off of the undersurface of the patella. If that occurs, the treating surgeon will scope the knee and either reattach or remove the broken piece of cartilage.
Patients with chronic patellar instability often have some degree of lower leg malalignment. Rehab can be attempted but is less successful in chronic cases. Multiple procedures have been developed to try and address recurrent patellar dislocations. The most successful operations involve trying to improve the alignment of the extensor mechanism. This allows the knee cap to stay in the trochlea during knee motion.
Proximal and Distal Realignment Procedures
For patients with chronic patellar instability, surgeons try to change the direction the kneecap travels during motion with hopes of eliminating dislocations. These procedures can be quite complicated depending on the amount of correction that the individual patient requires. Some basic surgical principles exist, however, despite the variation in specific techniques.
In most cases of patellar instability, the tissues on the inside of the patella are loose and the tissues on the outside are tight. Also, the alignment of the extensor mechanism is abnormal. The majority of surgical procedures for this condition attempt to correct these three factors. It is not uncommon for patients to spend a day or two in the hospital after surgery.
An arthroscopic lateral release is utilized to divide the tight tissues on the outside of the patella. This has been described previously. Next, in order to change the pull of the extensor mechanism, a realignment procedure is needed. This is reserved
for patients who have stopped growing. Realignment is typically accomplished by performing an osteotomy of the tibial tubercle. The tibial tubercle is the bony prominence on the front of the shin bone where the patellar tendon attaches. An osteotomy involves separating the tubercle from the tibia and shifting it in an inward direction. This requires an open incision and screws are usually placed to hold the shifted piece of bone in position. Lastly, some form of medial (inside) tightening procedure is performed. This usually requires a second incision on the inner portion of the knee. Sutures are utilized to tighten tissues on the inside of the patella that have become loose from multiple dislocations.
The postoperative rehabilitation for a proximal/distal realignment procedure involves a period of protected weight-bearing with crutches to allow the osteotomized bone to heal. A brace is worn to protect the knee for 4-6 weeks. Range of motion exercises are initiated early. Return to sports is permitted 4-6 months after surgery.
Plica
A plica is a band of synovium (lining of the inside of the knee) that is a normal remnant of embryologic tissue. Almost all knees have some form of plica, and they are often normal findings seen at the time of arthroscopy. Occasionally, however, patients can have symptomatic plicae. Plical pain is typically located on the inner portion of the knee next to the patella. Sometimes, popping or snapping can be elicited with knee motion.
Symptomatic plicae can be treated conservatively with medications, activity modification, and therapy. Surgical management is reserved for plicae that are resistant to nonoperative treatment. Surgery is performed arthroscopically simply by removing the pathologic tissue with a shaver. Postop rehab is identical to that of basic knee arthroscopic procedures.
Fat Pad Impingement
The anterior fat pad is fatty tissue that is located below the patella and behind the patellar tendon. It serves to provide some extra cushion for the front of the knee. Sometimes, after trauma, this fat pad can become symptomatic. The fatty tissue can become thickened and irritated making it difficult for the patient to straighten their knee.
Treatment for fat pad impingement is usually conservative. Activity modification, rest, ice, and knee padding are helpful. Occasionally, arthroscopic excision is utilized in patients that fail conservative therapies. The abnormal fat pad is removed with an arthroscopic shaver. Postop rehab is identical to that of basic knee arthroscopic procedures.
Extensor Mechanism Disruption
The extensor mechanism consists of all the structures that allow for the leg to be straightened (extended). The quadriceps muscles coalesce into a central tendon that inserts on the top of the patella. The patellar tendon is a band of tissue that connects the bottom of the patella to the tibial tubercle on the shin bone. Both of these tendons can be sites of knee pathology.
Quadriceps and patellar tendon ruptures are somewhat common injuries. Typically, patients who experience this injury fall onto a partially bent knee. When the quadriceps muscle contracts to break the fall, the quadriceps tendon or patellar tendon cannot withstand the force and ruptures. This injury is most common in middle-aged patients who are part-time athletes (weekend warriors). After sustaining a quadriceps or patellar tendon tear, the patient experiences knee pain, swelling, and is unable to straighten the leg from a bent position.
Treatment for quadriceps and patellar tendon ruptures is almost always surgical. The tendon tears off of the bone and it needs to be reattached. This involves an open incision on the front of the knee. The edges of the torn tendon are cleaned up and sewn back to the kneecap with large caliber nonabsorbable suture that is placed through small drill holes in the patella. After surgery, patients are put in a knee brace locked in extension. Patients can walk and bear weight on crutches with the leg in an extended position. Range of motion rehab is started after a few weeks of immobilization to protect the repair.
Expected Outcomes
A wide spectrum of pathology can be treated with knee surgery. Results of surgical intervention vary based on the patient’s individual diagnosis and treatment rendered. Most operative procedures offer good results in most cases. Exceptions always occur. It is important for the patient to have a thorough discussion preoperatively with their treating surgeon so they have a complete understanding of the expected goals and outcomes for their specific condition. Patient compliance and dedication to postoperative rehabilitation are also essential factors to maximize results following knee surgery.
Complications
Despite considerable progress in the field of knee surgery, surgical complications still exist. Every operation, as small as it may be, carries a wide range of risks from the most insignificant to the most serious (including fatal complications). Surely, discussing these complications with a patient does not mean that they will occur, but, by the same token, the failure to discuss these potential complications with the patient will not make them disappear. Patients are encouraged to ask their surgeon about potential complications, and the surgeon’s response should be forthcoming. Knee conditions are not life or death situations. Knee surgery pertains to quality of life. Therefore, it is essential for the patient to determine whether surgery is reasonable. To reach such a decision, the patient will use the information provided by the surgeon. The list of potential complications is extensive. Fortunately, complications are usually rare and benign.
The incidence of complications is low compared to the high number of arthroscopic procedures performed yearly. Possible complications include infection, swelling, damage to the tissues in the joint, blood clots in the leg veins (thrombophlebitis), accumulation of blood in the joint (hemarthrosis), blood clots that move to the lung (pulmonary embolus), and injury to the nerves around the joint.
Summary
Arthroscopic knee surgery is the most common procedure performed by orthopaedic surgeons. A large number of conditions can be treated successfully with arthroscopic techniques. The specific goals of each procedure vary based on individual diagnosis, but common themes include pain relief and restoration of form and function for patients.
Source
http://knol.google.com/k/knee-surgery#
http://knol.google.com/k/knee-surgery#
Justin D. Harris, MD
Orthopaedic Surgeon
Lincoln, NE
This knol provides a general overview of sports-related knee injuries. It is intended to provide basic information for patients and other healthcare professionals regarding the most commonly treated knee conditions.
Mechanism of injury, symptomatology, treatment options, and basic rehabilitation principles are discussed for each condition.
Introduction
Knee injuries and knee pain are extremely common. Knee problems are the most common reason patients need to see an orthopaedic surgeon. The knee is an extremely complex joint that is subjected to large forces during daily and athletic activities. Sports injuries frequently involve the knee, and as we age, degenerative knee problems develop. Many knee injuries can be treated conservatively (without surgery), but certain knee conditions benefit from surgical intervention.
Anatomy and Function
The knee is the largest joint in the body. Knee function primarily involves bending (flexion) and straightening (extending) the leg. Rotation also occurs within the knee. Anatomically, it is composed of the lower end of the thigh bone (distal femur) and upper end of the shin bone (proximal tibia). The front of the knee is covered by the knee cap (patella) that slides in a groove in the distal femur (trochlea) during knee motion.
The ends of the femur and the tibia, as well as the undersurface of the patella, are covered with cartilage. This cartilage has been described as the “white on the end of a chicken bone.” This “articular cartilage” serves to help with joint motion by providing lubrication and minimizing friction. Deterioration or wear of this articular cartilage is termed arthritis.
The knee also contains two “shock-absorber” pieces of cartilage called menisci. The medial meniscus sits between the femur and the tibia on the inner part of the knee, whereas the lateral meniscus occupies the outer part of the joint. Meniscal function is to provide cushion for the bones of the knee.
Knee stability is provided the ligaments of the knee. The cruciate ligaments (ACL and PCL) are in the center of the knee and serve to resist translational and rotational moments about the knee. The medial collateral ligament (MCL) is on the inner part of the knee connecting the femur and the tibia. The lateral collateral ligament (LCL) is on the outer part of the knee. The collateral ligaments resist side-to-side movements about the knee.
Lastly, the quadriceps tendon and the patellar tendon make up the extensor mechanism of the knee. The quadriceps are the muscles on the front of the thigh. At the knee, they form a tendon that inserts on the knee cap. There is a second tendon that runs from the knee cap to the top of the tibia (shin bone). These tendons as well as the patella allow us to straighten the knee from a bent position.
www.aclsolutions.com
http://www.leadingmd.com/patientEd/meniscus/overview.asp
Orthopaedic Knee Evaluation
The orthopaedic knee evaluation typically involves a detailed medical history, a thorough knee examination, and imaging studies. The medical history involves questions about the patient’s health as well as details regarding their knee symptoms. Important factors to consider are the duration and intensity of symptoms. The location and quality of the pain are also important. Knee conditions may often involve swelling, mechanical symptoms (popping, catching, locking), and sensations of instability. Alleviating and aggravating factors are important to mention.
The knee evaluation involves checking the back and the hip to ensure that the pain is coming from the knee. Inspection of the muscles and the alignment of the leg is next. Range of motion and walking observation follow. The surgeon will then palpate specific areas of tenderness to try to determine the location of the pathology. Lastly, specific tests are performed to assess the quality of various tissues in and about the knee (menisci and ligaments).
Most surgeons will order x-rays to look at the bony structures of the knee. Fractures, leg malalignment, and arthritis will often be noted on x-rays. Soft tissue structures (cartilage, menisci, and ligaments) are best evaluated with an MRI.
After compiling all the information from the history, physical examination, and imaging studies, the orthopaedic surgeon will make a diagnosis and present
a treatment plan. Treatment options may include medications, physical therapy, or orthotics. Surgery may be recommended. The surgeon will then describe the surgical procedure, explain the risks and benefits associated with the procedure, and detail the expected postoperative recovery.
Knee Surgery
Various injuries and conditions within the knee are treated operatively. Indications for surgical treatment vary, based on individual diagnosis. Certain conditions may fail to respond to conservative management, whereas other injuries are treated more aggressively. The goal of all treatment is to try to return the patient to their previous level of activity and function.
Knee surgery can be performed arthroscopically or in an open fashion. Arthroscopic surgery allows an orthopaedic surgeon to diagnose and treat knee injuries by viewing the inside of the knee through small incisions using a pencil-sized instrument called an arthroscope. The knee is filled with fluid and the scope transmits an image of the knee through a camera to a television monitor. During the procedure, additional small incisions are created to allow insertion of other small instruments to remove or repair damaged tissues. Most arthroscopic knee procedures are done as an outpatient. Recovery is typically much quicker and easier than traditional open knee procedures.
Open knee surgery involves larger incisions to enter the knee joint (arthrotomy).
These operations are more extensive and often more complex than most arthroscopic procedures. They may be done as an outpatient, but a short inpatient stay afterward is not uncommon.
Rehabilitation for knee injuries and after knee surgery varies based on the patient’s specific injury complex and the surgical procedure that was performed. Physical therapy can be utilized as a nonoperative modality for a number of knee conditions. The primary goals of PT for knee pain include maximizing range of motion, improving flexibility, and strengthening the muscles around the knee to take stress off of injured tissues.
Postoperative rehab can be quite variable. Some simple knee surgeries don’t require formal therapy at all, whereas other procedures require months of dedicated physical therapy to achieve maximum results.
A more detailed description of individual surgical procedures and the expected postoperative recovery follows.
Meniscal Injuries
Meniscal injuries are the most commonly surgically-treated knee condition. The menisci are shock-absorber cartilage between the femur and the tibia. The medial meniscus is on the inner portion of the knee, whereas the lateral meniscus is on the outer part of the knee. Young patients typically sustain meniscal injuries during athletic activities. Cutting and pivoting can stress the meniscus to the point that it tears. Older patients tear their menisci during less vigorous activities. As we age, the meniscus starts to degenerate and can tear with trivial trauma. A large percentage of older patients actually have asymptomatic meniscal tears.
Symptoms of a torn meniscus include recurrent swelling (effusions), mechanical symptoms (popping, catching, and locking), and pain with deep squatting. The pain is typically localized to one side of the knee or the other. A medial meniscus tear hurts on the inside of the knee, while a lateral meniscal tear hurts on the outside. Cutting, pivoting, and athletic activities may be difficult with a meniscus tear.
Surgery for a torn meniscus is typically done arthroscopically. The specific surgical procedure that is performed is dependent on a number of factors. It is important to try to preserve meniscal tissue because arthritis tends to develop faster in knees that have less meniscus remaining.
Meniscus tears that occur in young patients and are located near the edge of the meniscus (best blood supply) are often repairable. Meniscus tears near the central surface and those that occur in older patients are often removed (partial meniscectomy) because they lack the capacity to heal. In some select situations, patients that have had a significant portion of their meniscus removed may be a candidate for a meniscal transplant, where a cadaver meniscus is placed in the knee to try to prevent joint degeneration.
Partial Meniscectomy
Arthroscopic partial meniscectomy is the most common arthroscopic procedure that surgeons perform. Patients that have symptomatic meniscal tears are usually good candidates for arthroscopic surgery. If a surgeon determines that a meniscal tear is unlikely to heal, the torn meniscal tissue is removed surgically. This is called a partial meniscectomy. (Fi
Partial meniscectomies are performed arthroscopically. Once the torn tissue has been removed from the knee, patients typically feel much improved. The postoperative course is fairly straightforward. Most patients are on crutches for a couple of days to help stabilize the knee. Once the swelling subsides, the rehabilitation progresses quickly. Most patients can return to work after only a few days. Return to sports is permitted once the swelling is gone, and the patient has normal quadriceps function.
Video of a partial medial meniscectomy
More video of a partial medial meniscectomy
Meniscal Repair
Meniscus repairs are typically reserved for younger patients (< 40 years of age) who have a tear that is located near the outer rim of the meniscus. The goal of all meniscal surgery is to preserve meniscal tissue, but repairs are only indicated where healing can be expected.
Surgeons employ various meniscal repair techniques. The basic principles involve placing suture or some type of bioabsorbable implant across the tear, which will stabilize it until it heals. Smaller tears are amenable to repairs with meniscal fixation devices placed arthroscopically (all-inside). Larger tears occasionally require a secondary incision on the side of the knee (inside-out). Results of successful healing after meniscal repair vary from 60%-80%.
The postoperative rehabilitation following a meniscal repair will vary based on surgeon preference, but basic guidelines are usually followed. The meniscus typically takes a few months to be fully healed so the repair must be protected during that time. Most patients are placed in a hinged-knee brace at the time of surgery. They can bear weight within the brace but usually only locked in full extension (leg straight). Range-of-motion exercises are allowed but higher degrees of flexion are usually avoided (< 90).
After the first month the brace is unlocked during weight bearing, and higher knee flexion is permissible. Most patients are allowed to return to sports anywhere from 3 to 6 months after surgery, depending on the severity of the tear.
Ligament Injuries
There are four main ligaments around the knee. The ACL, PCL, MCL, and LCL have been described previously. Injuries to these structures are not uncommon. As we have become a more active and a more sports-oriented society, the incidence of knee ligament injuries has increased. Treatment of knee ligament injuries is based on multiple factors. Each individual ligament is treated differently. Patient age, health, and activity level all play a role in determining optimal treatment. Additional pathology within the knee can also alter the treatment plan.
Anterior Cruciate Ligament Injuries
ACL injuries occur through some form of twisting mechanism. This can occur while the foot is planted on the ground or after landing awkwardly from a jump. Additionally, a “contact” injury can occur where the knee is forced in an abnormal position by an outside stress.
Acute symptoms of an ACL injury include hearing or feeling “a pop.” Swelling of the knee can develop quite quickly. In chronic settings, knee instability becomes more common, especially during cutting and pivoting activities.
The treatment of ACL injuries is dictated by the patient’s activity level and expectations. Patients who live a sedentary lifestyle may not need to have their ACL tear treated surgically. However, athletes who wish to regain the ability to participate in cutting and pivoting sports will likely benefit from ACL surgery.
Anterior Cruciate Ligament Reconstruction
Anterior cruciate ligament tears usually cannot be repaired. As such, a reconstruction or “ACL replacement” must be performed. The most common type of ACL reconstruction involves taking tissue and creating a new ligament which is then placed within the knee. This serves to replace the torn ACL.
The most concerning issue for patients undergoing ACL reconstruction is the graft source. The new ACL can come from the patient (autograft) or it can come from a cadaver (allograft). There are risks and benefits to both options. The most common autograft options are patellar tendon and hamstrings.
ACL reconstruction is typically done as an outpatient procedure. Depending on graft choice, open incisions may be necessary to harvest the tissue that is to be used as the new ACL. Knee arthroscopy is then performed to inspect the knee, treat additional injuries (meniscus tears or cartilage damage), and to prepare the knee for the new ACL.
Once the graft tissue has been prepared and the torn ACL tissue has been removed, the surgeon is ready to place the ligament within the knee. Small tunnels (7-10 mm) are drilled in the tibia and the femur to allow the ligament to be pulled up into the knee.
Accurate placement of these tunnels is critical to successful ACL surgery. After the ACL graft is in position, fixation devices (screws, washers, buttons, etc.) are used to keep it there until it can heal into place.
Rehabilitation after ACL reconstruction is a necessary part of a successful procedure. The patient is placed in a brace after surgery. Therapy is started shortly thereafter. Weight bearing is typically allowed immediately. Maintaining full extension and minimizing swelling are early goals. Range of motion activities then begin. Strengthening of the leg comes next, with gradual return to straight ahead running. Sport specific rehab and cutting and pivoting are the last steps prior to return to athletics. The typical athlete is held out of sports for 6 months following ACL reconstruction.
Posterior Cruciate Ligament Injuries
Posterior cruciate ligament (PCL) injuries are much less common than ACL tears. The most common mechanism of injury involves a direct blow to the front of the tibia. This can occur during sports or in motor vehicle collisions. The tibia is forced backwards relative to the femur and the PCL tears. Other common athletic mechanisms include knee hyperextension and forced knee flexion with the foot plantar flexed. Acutely, PCL tears can present similarly to other knee injuries. Swelling, pain, and instability are common. In the chronic setting, persistent instability may occur.
Management of isolated PCL tears is typically conservative. Once the acute swelling and discomfort of the initial trauma subsides, physical therapy is utilized to try and maximize quadriceps strength to assist with dynamic knee stability. After completion of a dedicated rehab program, the patient is allowed to return to play once full motion and near-normal strength have returned.
Posterior Cruciate Ligament Reconstruction
PCL surgery is much less common than ACL surgery. Surgical intervention is typically reserved for specific indications. PCL tears that pull a piece of bone off of the tibia (avulsion fracture) may benefit from operative fixation. PCL injuries that occur in conjunction with other knee ligament tears (knee dislocations) often benefit from surgical reconstruction. Finally, patients who have had PCL tears treated conservatively, but still complain of instability are candidates for PCL reconstruction.
PCL reconstruction involves taking tissue from another source and creating a new PCL. Autograft or allograft sources can be used to make the PCL graft. Graft choice is determined after a discussion of risks and benefits of each option between the patient and the treating orthopaedic surgeon. Isolated PCL reconstruction can often be done as an outpatient procedure, whereas multiple ligament knee surgery typically requires a short hospital stay. PCL surgery is usually done as an arthroscopic procedure, although some small open incisions are often required. An added degree of difficulty exists when compared with ACL reconstruction, because the PCL attachment site on the tibia can be more challenging to access. Just as in ACL reconstruction, the torn PCL is removed arthroscopically. Tunnels are then drilled in the tibia and the femur to allow passage of the PCL graft. The new PCL is then pulled into the knee and fixed to the bone.
Rehabilitation after PCL reconstruction varies based on surgeon preference. Braces are typically worn in the early postoperative period. Weight bearing may be delayed in some instances. Postoperative therapy focuses on quadriceps strengthening to prevent the tibia from sagging backward, which can stretch the PCL graft. Most patients return to sports and full activity 6-8 months after surgery
Medial Collateral Ligament Injuries
Medial collateral ligament (MCL) injuries occur when the knee buckles to the inside. This often happens when an athlete sustains a direct blow to the outside of the knee forcing it inward. Pain is felt on the inner (medial) part of the knee. Noncontact injuries often result in isolated partial MCL tears, whereas contact mechanisms can produce complete MCL tears and may injure other knee ligaments as well (ACL).
The most common symptom following a medial collateral ligament injury is pain directly over the ligament. Swelling over the torn ligament may appear, and bruising and generalized joint swelling are common 1 to 2 days after the injury. In more severe injuries, patients may complain that the knee is unstable, or feel as though their knee may “give out” or buckle.
The majority of MCL injuries are treated conservatively (without surgery). The duration of convalescence is dependent on the severity of the injury. Partial MCL tears usually heal quickly and athletes return to play within a couple of weeks. Minimizing swelling and maintaining range of motion are essential to facilitate a quick recovery. Complete MCL tears may take more than 6 weeks to heal. Pain, swelling, and stiffness are common. Bracing is usually utilized to help the ligament heal under normal tension. Range of motion exercises are emphasized during rehab to prevent knee stiffness from developing. Complete rehab from a full thickness MCL tear can take 3-4 months in some situations.
http://www.kneeguru.co.uk/html/steps/step_03_collaterals/injury.html
Medial Collateral Ligament Repair/Reconstruction
As stated previously, most MCL injuries don’t require surgery. However, certain surgical indications do exist. High-grade (complete) MCL tears that coexist with other knee ligament injuries may benefit from surgical repair. Additionally, MCL tears that have healed with residual laxity (looseness), causing persistent instability of the knee, often benefit from repair or reconstruction.
MCL surgery is done via an open incision on the inner portion of the knee. If the operation is done in the acute setting (< 3 weeks after injury), primary repair of the torn ligament is possible. Midsubstance ruptures are reapproximated (connected) and sutured together with large caliber permanent suture material. Tears that pull of off the ligament’s bony attachment sites are usually put back down to the bone with suture anchors.
In cases of chronic MCL laxity and instability, MCL reconstruction is often necessary. In these instances, a new MCL is fashioned from autograft or allograft tissue. The new ligament is then placed over the top of the old MCL and secured to the femur and the tibia with fixation devices.
Rehabilitation after MCL surgery is similar to that of other knee ligament postoperative protocols. The knee is protected in a brace for a few weeks after surgery. Range of motion exercises are initiated early to prevent stiffness. Strengthening begins 6-8 weeks after surgery. Complete rehab takes 4-6 months.
Lateral Collateral Ligament/Posterolateral Corner Injuries
Lateral collateral ligament (LCL) injuries occur when the knee buckles outward. These are typically high-energy contact injuries where a force is applied to the inner part of the knee which then stretches or tears the ligament on the outside. Pain is felt on the outer part of the knee over the LCL. Symptoms are similar to other knee ligament injuries.
Isolated LCL injuries do well with conservative management. Rest, icing, and early motion permit a relatively quick return to sports and activity. Unfortunately, injuries to the lateral side of the knee often produce more trauma than just isolated LCL tears. The posterolateral corner (PLC) is a complex of ligamentous structures behind the LCL that serve to resist varus (outward) stress, posterior (backward) displacement of the tibia, as well as external rotation of the knee. PLC injuries typically occur in conjunction with other knee ligament injuries. They are often misdiagnosed and can play a role in why other ligament surgery (ACL/PCL) fails.
Lateral Collateral Ligament/Posterolateral Corner Repair/Reconstruction
Surgery for the LCL/PLC is typically reserved for knees with multiple ligaments that are injured. Common combinations include ACL/PLC injuries and PCL/PLC injuries. Knee dislocations often have PLC involvement as well. In most settings, if the LCL/PLC is ignored, the results of cruciate reconstruction will be diminished. Lateral-sided knee injuries are repaired through open incisions. For acute injuries, primary repair of the PLC is possible. The tendons and ligaments that are injured are sutured together primarily or are reattached back to their insertion points on the bony structures. In the chronic setting, the LCL and PLC have healed and scarred together with residual laxity. Primary repair is not possible. As such, reconstruction is then performed with autograft or allograft tissue. Multiple reconstruction techniques have been described. Postoperative management is similar to that described above.
Articular Cartilage Injuries
Articular cartilage is the smooth, glistening, white tissue that covers the ends of bones in the human body. It functions to resist compressive loads in joints and provides a smooth surface with low friction to allow for supple joint movement. Injury to articular cartilage is extremely common. Traumatic events can damage cartilage, and as we age, the biology of the cartilage changes, predisposing it to wear and injury. Cartilage injuries are concerning because articular cartilage lacks a blood supply, which prevents it from healing.
Articular cartilage injuries can occur as a result of either traumatic mechanical destruction, or progressive mechanical degeneration (wear & tear). ACL tears, patellar dislocations, and other knee injuries can present with acute articular cartilage damage. Typically, these mechanisms of injury create small, focal defects in the cartilage. Degenerative cartilage lesions can be shallower but often involve more overall surface area. Additionally, osteochondritis dissecans (OCD) is a condition where the bone behind the articular cartilage is diseased, which may lead to a large defect if a piece of cartilage were to detach from the underlying bone.
Symptoms of articular cartilage damage include knee swelling and vague pain. Mechanical symptoms (catching and locking) may also be present. With mechanical degeneration (wear and tear), the patient often experiences stiffness, decreased range of motion, joint pain and/or swelling.
Cartilage injury is difficult to diagnose by history and physical exam alone. Radiographs (x-rays) and an MRI of the knee are helpful to evaluate the health of the cartilage. X-rays are used to look for moderate to severe signs of arthritis (diffuse cartilage degeneration). MRI is helpful to look for focal cartilage lesions as well as to look for loose bodies (pieces of cartilage that have detached and are floating in the knee) and additional pathology within the knee.
Treatment of articular cartilage lesions is dependent on multiple factors. Patient age, activity level, and mechanism of injury commonly dictate management. Young patients with traumatic injuries are treated aggressively to try to restore a normal articular surface within the knee. Older patients with degenerative cartilage problems can initially be treated conservatively.
Nonoperative treatment is indicated for patients who present with diffuse osteoarthritis. Management consists of physical therapy, medications activity modification, orthotics, bracing, and injections. Failure of conservative management may be an indication for surgical intervention, depending on the patient’s symptomatology.
Operative management for cartilage injuries is reserved for acute traumatic defects, OCD lesions that are deemed to be unstable (at risk for detachment), and loose bodies within the knee. Small focal lesions can be treated conservatively, but this is usually unsuccessful. Large lesions should be treated aggressively to prevent joint deterioration. The specific surgical procedure to treat articular cartilage lesions is dictated by the lesion size, the quality of the bone behind the lesion, and surgeon preference.
Loose Body Removal
Loose bodies within the knee often cause symptoms of pain, catching, and locking. Symptomatic loose bodies should be removed. This is performed as an outpatient, arthroscopic procedure. The surgeon uses the arthroscope to find and localize the loose bodies and they are removed with an arthroscopic grasper. The remainder of the knee is evaluated and any additional pathology is treated appropriately.
Rehab after simple loose body removal is fairly straightforward. Crutches may be needed for a couple of days, but patients are allowed to return to full activity once swelling and range of motion have normalized.
Arthroscopic Chondroplasty
Arthroscopic chondroplasty is commonly performed during knee arthroscopy. It is utilized for treating incidentally-found chondral lesions during surgery. It can also be utilized for small areas of superficial cartilage damage in patients that experience joint pain and have associated mechanical symptoms. Loose cartilage flaps and debris within the knee are removed using an arthroscopic shaver. Great care is taken to avoid damaging normal cartilage. The goal of surgery is to eliminate catching and locking from these loose pieces of cartilage and to try to prevent propagation of these chondral flaps. The postoperative management is identical to that of basic knee arthroscopic procedures described previously.
Microfracture
Small, focal lesions (< 2 cm) of cartilage damage that are surrounded by healthy tissue are often treated with a microfracture procedure. As cartilage has no blood supply, it lacks the ability to heal. The bone beneath the cartilage, however, has a rich blood supply. Microfracture procedures try to access the osseous vascular supply in order to heal cartilage defects. Microfracture creates small holes in the bone at the base of a cartilage lesion. This allows cells from the bone marrow to fill in the defect and stimulate new cartilage growth. This new cartilage is a scar-type of cartilage called fibrocartilage. It is less durable than normal hyaline cartilage, but provides a smooth covering of the lesion.
Indications for microfracture are small to moderately-sized focal cartilage lesions. Widespread cartilage damage is a contraindication to a microfracture procedure. It is done arthroscopically. The cartilage defect is evaluated and measured by the surgeon. Loose cartilage flaps are removed with a shaver. Then, a small, sharp pick (awl) is used to create the small microfracture holes in the bone. The number of microfracture holes created depends on the size of the area being treated. Most patients with a 1- to 2-centimeter area of damage require 5 to 15 small holes in the bone.
The postoperative management of a microfracture procedure is critical. Surgery is typically done as an outpatient. The patient is kept non-weight bearing and on crutches for 6-8 weeks following surgery. Range of motion is essential after surgery to allow the fibrocartilage to grow and mature into a normal shape. Many surgeons will use a CPM (continuous passive motion) machine after surgery to facilitate this. Microfracture done in the area of the kneecap (patellofemoral joint) is rehabilitated somewhat differently, in that motion is restricted to avoid excess pressure placed on the healing area.
Autologous Chondrocyte Implantation
Another option for attempting to heal cartilage lesions is autologous chondrocyte implantation (ACI). This procedure is reserved for patients with small to moderate-sized lesions who have usually failed a previous procedure (chondroplasty or microfracture). The procedure is complex, and the rehab is extensive so appropriate patient selection is critical. It is a two-stage operation in which cartilage cells are harvested from the knee, grown in a lab, and then reimplanted into the knee during a second operation.
The first step of an ACI surgery is to perform an arthroscopic procedure where the cartilage defect is evaluated. If the lesion is appropriate for ACI (based on size, depth, and quality of the surrounding cartilage), small pieces of normal cartilage are harvested from less essential areas of the knee. This cartilage is then sent to a cartilage expansion laboratory where the cells are cultured and multiplied. Once enough cells have been grown, the second stage of the operation is scheduled.
The second stage of ACI surgery involves implantation of the cartilage cells. This is done as an open procedure. The area of cartilage damage is exposed and sized. A second incision is then made over the shin and a “patch” is harvested from the thick tissue (periosteum) that covers the shin bone. This patch is roughly the size of the cartilage lesion being treated. The patch is then sewn over the cartilage defect and the cultured cells are injected underneath the periosteal patch.
The rehab after ACI is similar to that of microfracture. Weight-bearing is restricted and crutches are required for 6-8 weeks while the cells adhere to the underlying bone. Motion is encouraged, often with the use of a CPM. Training intensity increases from 3-6 months postoperatively, but most athletes don’t return to sports for 12-16 months following surgery.
Osteochondral Autograft Transfer
Another surgical option for symptomatic, focal articular cartilage lesions is an osteochondral autograft transfer. This is also referred to as a mosaicplasty, or an OATS procedure. Mosaicplasty involves harvesting normal cartilage from the knee and transferring it to replace the area of damaged cartilage.
Indications for mosaicplasty are similar to that of ACI. Lesions < 2 cm in diameter are ideal. This is not a procedure utilized to treat diffuse cartilage damage. The surgery can be done arthroscopically or open. It is commonly performed as an outpatient. The cartilage defect is usually evaluated and prepared arthroscopically. If the lesion is appropriate for mosaicplasty, appropriately-sized osteochondral plugs are harvested from another part of the knee joint. The cartilage in this “donor area” is not as essential because it is subjected to less pressure during weight-bearing. The plugs are then transferred to the cartilage defect and set into place.
The rehab after osteochondral autograft transfer is similar to that described previously. Weight bearing is restricted for 6-8 weeks. Motion is encouraged. Return to sports and full activity is permitted after 6 months of rehab in most cases.
Osteochondral Allograft Transplantation
Large, focal cartilage lesions (> 2 cm in diameter) are often too large to be treated with microfracture, ACI, or mosaicplasty. For these patients, an allograft is often the only tissue source large enough to provide enough cartilage to cover the defect. An allograft is donated tissue that comes from a cadaver. Patients who are candidates for allograft transplantation have their imaging studies (x-rays or MRI) sent to a tissue bank which tries to procure a graft that is size matched to the patient. When a graft is found, surgery is scheduled.
Osteochondral allograft transplantation is typically done as an open procedure. A short hospital stay is not uncommon. The area of damaged cartilage is prepared by coring a socket 4-5 mm deep into the subchondral bone. The exact same location is then identified on the allograft specimen and a plug is created that fits perfectly into the host femur. The allograft plug is then placed within the recipient socket. The goal is to create a flush, smooth surface of articular cartilage.
The postoperative management of osteochondral allograft transplantation is slower than that of other cartilage restoration procedures. The bony portion of the graft needs to be replaced by bone from the patient, and while this occurs the graft is susceptible to collapse. As a result, weight-bearing is restricted for 10-12 weeks. Motion is encouraged early. Patients are allowed to return to full activity 12 months after surgery.
Patellofemoral Disorders
The patellofemoral joint is the articulation between the undersurface of the kneecap (patella) and the groove in the front of the femur (trochlea). It is a common source of pain and disability in patients. Patellofemoral issues commonly present as pain in the front of the knee (anterior knee pain). Aggravating factors include stair climbing and standing up from a seated position. Multiple conditions can present with patellofemoral pain, which can make determining optimum treatment difficult. Fortunately, most anterior knee pain responds to conservative management, but specific surgical indications do exist for some conditions. More detailed descriptions of these conditions follow.
Lateral Patellar Compression Syndrome
Lateral patellar compression syndrome (LPCS) is a common condition that presents with anterior knee pain. It is characterized by a tight lateral retinaculum (tissue on the outside of the patella). This tight tissue causes abnormal motion of the patella within the trochlea. This can be exacerbated by other patient factors, such as limb alignment and muscle strength. Patients with LPCS have limited medial (inside) mobility of the patella and may have a patella with excessive lateral tilt.
Conservative management is indicated in all cases of LPCS. Physical therapy is the mainstay of treatment. Quadriceps strengthening, flexibility training, and patellar taping all can be beneficial. A patellar sleeve or brace can also be helpful during athletic activities. A dedicated course of nonoperative treatment needs to be attempted before considering surgical intervention for LPCS.
Lateral Release
The most common surgical intervention for LPCS is a lateral release. This procedure involves surgically dividing the tight lateral retinaculum that is tethering the patella. It is most often done arthroscopically as an outpatient procedure. There is a mild risk of excessive bleeding within the knee after the release. Results for this procedure are good if strict surgical indications are followed. The rehab postoperatively involves minimizing swelling initially, followed by dedicated quadriceps strengthening.
Patellar Instability
Patellar instability occurs when the kneecap slides out of its groove (trochlea) as the knee bends. Most commonly, the patella displaces (dislocates) in a lateral direction (toward the outside). Patellar instability can be described as acute or chronic. Acute patellar dislocations occur when a twisting force is applied to the lower leg. The femur rotates inward while the tibia and the patella rotate outward. This can result in a patellar dislocation.
Chronic patellar instability occurs in patients that have developed specific anatomic risk factors. A wide pelvis, a shallow trochlea, a high-riding patella, knock-knees, flat feet, and underdeveloped thigh musculature are all risk factors for recurrent patellar instability.
The treatment of acute patellar dislocations is typically nonsurgical. A brief period of immobilization (4 weeks) is followed by a dedicated rehabilitation program. Rehab should focus on quadriceps strengthening exercises and flexibility training. The primary surgical indication for an acute patellar dislocation is when a piece of cartilage breaks off of the undersurface of the patella. If that occurs, the treating surgeon will scope the knee and either reattach or remove the broken piece of cartilage.
Patients with chronic patellar instability often have some degree of lower leg malalignment. Rehab can be attempted but is less successful in chronic cases. Multiple procedures have been developed to try and address recurrent patellar dislocations. The most successful operations involve trying to improve the alignment of the extensor mechanism. This allows the knee cap to stay in the trochlea during knee motion.
Proximal and Distal Realignment Procedures
For patients with chronic patellar instability, surgeons try to change the direction the kneecap travels during motion with hopes of eliminating dislocations. These procedures can be quite complicated depending on the amount of correction that the individual patient requires. Some basic surgical principles exist, however, despite the variation in specific techniques.
In most cases of patellar instability, the tissues on the inside of the patella are loose and the tissues on the outside are tight. Also, the alignment of the extensor mechanism is abnormal. The majority of surgical procedures for this condition attempt to correct these three factors. It is not uncommon for patients to spend a day or two in the hospital after surgery.
An arthroscopic lateral release is utilized to divide the tight tissues on the outside of the patella. This has been described previously. Next, in order to change the pull of the extensor mechanism, a realignment procedure is needed. This is reserved
for patients who have stopped growing. Realignment is typically accomplished by performing an osteotomy of the tibial tubercle. The tibial tubercle is the bony prominence on the front of the shin bone where the patellar tendon attaches. An osteotomy involves separating the tubercle from the tibia and shifting it in an inward direction. This requires an open incision and screws are usually placed to hold the shifted piece of bone in position. Lastly, some form of medial (inside) tightening procedure is performed. This usually requires a second incision on the inner portion of the knee. Sutures are utilized to tighten tissues on the inside of the patella that have become loose from multiple dislocations.
The postoperative rehabilitation for a proximal/distal realignment procedure involves a period of protected weight-bearing with crutches to allow the osteotomized bone to heal. A brace is worn to protect the knee for 4-6 weeks. Range of motion exercises are initiated early. Return to sports is permitted 4-6 months after surgery.
Plica
A plica is a band of synovium (lining of the inside of the knee) that is a normal remnant of embryologic tissue. Almost all knees have some form of plica, and they are often normal findings seen at the time of arthroscopy. Occasionally, however, patients can have symptomatic plicae. Plical pain is typically located on the inner portion of the knee next to the patella. Sometimes, popping or snapping can be elicited with knee motion.
Symptomatic plicae can be treated conservatively with medications, activity modification, and therapy. Surgical management is reserved for plicae that are resistant to nonoperative treatment. Surgery is performed arthroscopically simply by removing the pathologic tissue with a shaver. Postop rehab is identical to that of basic knee arthroscopic procedures.
Fat Pad Impingement
The anterior fat pad is fatty tissue that is located below the patella and behind the patellar tendon. It serves to provide some extra cushion for the front of the knee. Sometimes, after trauma, this fat pad can become symptomatic. The fatty tissue can become thickened and irritated making it difficult for the patient to straighten their knee.
Treatment for fat pad impingement is usually conservative. Activity modification, rest, ice, and knee padding are helpful. Occasionally, arthroscopic excision is utilized in patients that fail conservative therapies. The abnormal fat pad is removed with an arthroscopic shaver. Postop rehab is identical to that of basic knee arthroscopic procedures.
Extensor Mechanism Disruption
The extensor mechanism consists of all the structures that allow for the leg to be straightened (extended). The quadriceps muscles coalesce into a central tendon that inserts on the top of the patella. The patellar tendon is a band of tissue that connects the bottom of the patella to the tibial tubercle on the shin bone. Both of these tendons can be sites of knee pathology.
Quadriceps and patellar tendon ruptures are somewhat common injuries. Typically, patients who experience this injury fall onto a partially bent knee. When the quadriceps muscle contracts to break the fall, the quadriceps tendon or patellar tendon cannot withstand the force and ruptures. This injury is most common in middle-aged patients who are part-time athletes (weekend warriors). After sustaining a quadriceps or patellar tendon tear, the patient experiences knee pain, swelling, and is unable to straighten the leg from a bent position.
Treatment for quadriceps and patellar tendon ruptures is almost always surgical. The tendon tears off of the bone and it needs to be reattached. This involves an open incision on the front of the knee. The edges of the torn tendon are cleaned up and sewn back to the kneecap with large caliber nonabsorbable suture that is placed through small drill holes in the patella. After surgery, patients are put in a knee brace locked in extension. Patients can walk and bear weight on crutches with the leg in an extended position. Range of motion rehab is started after a few weeks of immobilization to protect the repair.
Expected Outcomes
A wide spectrum of pathology can be treated with knee surgery. Results of surgical intervention vary based on the patient’s individual diagnosis and treatment rendered. Most operative procedures offer good results in most cases. Exceptions always occur. It is important for the patient to have a thorough discussion preoperatively with their treating surgeon so they have a complete understanding of the expected goals and outcomes for their specific condition. Patient compliance and dedication to postoperative rehabilitation are also essential factors to maximize results following knee surgery.
Complications
Despite considerable progress in the field of knee surgery, surgical complications still exist. Every operation, as small as it may be, carries a wide range of risks from the most insignificant to the most serious (including fatal complications). Surely, discussing these complications with a patient does not mean that they will occur, but, by the same token, the failure to discuss these potential complications with the patient will not make them disappear. Patients are encouraged to ask their surgeon about potential complications, and the surgeon’s response should be forthcoming. Knee conditions are not life or death situations. Knee surgery pertains to quality of life. Therefore, it is essential for the patient to determine whether surgery is reasonable. To reach such a decision, the patient will use the information provided by the surgeon. The list of potential complications is extensive. Fortunately, complications are usually rare and benign.
The incidence of complications is low compared to the high number of arthroscopic procedures performed yearly. Possible complications include infection, swelling, damage to the tissues in the joint, blood clots in the leg veins (thrombophlebitis), accumulation of blood in the joint (hemarthrosis), blood clots that move to the lung (pulmonary embolus), and injury to the nerves around the joint.
Summary
Arthroscopic knee surgery is the most common procedure performed by orthopaedic surgeons. A large number of conditions can be treated successfully with arthroscopic techniques. The specific goals of each procedure vary based on individual diagnosis, but common themes include pain relief and restoration of form and function for patients.
Source
http://knol.google.com/k/knee-surgery#
http://knol.google.com/k/knee-surgery#
Subscribe to:
Posts (Atom)