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Man CY, Cheung IT, Cameron PA, Rainer TH. Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial. Ann Emerg Med. 2007;49:670-677.
ILLUSTRATIVE CASE
A 68-year-old man with a history of ulcer disease and mild renal insufficiency comes to your office complaining of severe pain in his right foot. You note swelling and redness around the base of the big toe and diagnose acute gout. Wishing to avoid nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine because of the patient’s medical history, you wonder what you can safely prescribe for pain relief.
NSAIDs have become the mainstay of treatment for acute gout, (3,4) replacing colchicine–widely used for gout pain relief since the early 19th century. (5) Colchicine fell out of favor because it routinely causes diarrhea and requires caution in patients with renal insufficiency. (6) Now, however, there is growing concern about the adverse effects of NSAIDs.
* Comorbidities, age, mean fewer options
NSAIDs increase the risk of gastrointestinal (GI) bleeding, especially in the first week of use. (7) Cyclooxygenase-2 (C OX-2) inhibitors, considered as effective as NSAIDs in treating acute gout pain, (8) are also associated with GI bleeds. (9) In addition, NSAIDs and COX-2 inhibitors increase cardiovascular risks, prompting the American Heart Association to recommend restricted use of both. (10) NSAIDs’ effect on renal function, fluid retention, and interactions with anticoagulants are additional concerns, because gout patients are generally older and often have comorbid renal and cardiovascular diseases. (3, 11-13)
In the United States, nearly 70% of patients who develop acute gout seek treatment from primary care physicians. (12) Family physicians need a safe alternative to NSAIDs to relieve the severe pain associated with this condition. Will oral corticosteroids fit the bill?
STUDY SUMMARIES
* Oral steroids: A safe and effective alternative
Janssens et al (1) conducted a double-blind, randomized equivalence trial of 118 patients to compare the efficacy of prednisolone and naproxen for the treatment of monoarticular gout, confirmed by crystal analysis of synovial fluid. The study was conducted in the eastern Netherlands at a trial center patients were referred to by their family physicians. Those with major comorbidities, including a history of GI bleed or peptic ulcer, were excluded.
Participants were randomized to receive either prednisolone 35 mg * or naproxen 500 mg twice a day, with look-alike placebo tablets of the alternate drug, for 5 days. Pain, the primary outcome, was scored on a validated visual analog scale from 0 mm (no pain) to 100 mm (worst pain experienced). (15) The reduction in the pain score at 90 hours was similar in both groups. Only a few minor side effects were reported in both groups, and all completely resolved in 3 weeks.
The study by Man et al (2) was a randomized trial that compared indomethacin with oral prednisolone in 90 patients presenting to an emergency department in Hong Kong. Diagnosis of gout was made by clinical impression. Participants in the indomethacin group also received an intramuscular (IM) injection of diclofenac 75 mg, and those in both groups were monitored for acetaminophen use as a secondary endpoint.
Pain reduction, the primary endpoint, was assessed with a 10-point visual analog score, and was slightly better statistically in the oral steroid group. The study was not designed to evaluate for safety, but the authors noted that patients in the indomethacin group experienced more adverse effects (number needed to harm [NNH] for any adverse event: 3; NNH for serious events: 6).
Short-term steroids have few side effects
In both studies, patients receiving oral steroids experienced no significant side effects. This finding is consistent with other studies that have investigated short-term oral steroid use in the treatment of both rheumatoid arthritis and asthma. (16,17)
WHAT’S NEW?
* Evidence supports use of steroids for acute gout
In the United States, prednisone is prescribed as treatment for acute gout only about 9% of the time. (12) These 2 studies–the first randomized trials comparing oral steroids with NSAIDs, the usual gout treatment–may lead to greater use of steroids for this painful condition.
Both studies were well designed and conducted in an outpatient (or emergency) setting. Both showed that a short course of oral steroids is as effective as NSAIDs, and without significant side effects.

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In an animal model of indomethacin- and stress-induced upper-gastrointestinal damage, oral zinc L-carnosine decreased stomach injury by 75% and small intestinal injury by 50%. While adult volunteers who took indomethacin (50 mg, three times daily) for five days had increased gut permeability–a pathological change that may contribute to inflammation–no significant increase in intestinal permeability was seen when zinc L-carnosine (37.5 mg, twice daily) was co-administered. People who take NSAIDs may thus be able to guard their gastrointestinal health using supplemental zinc L-carnosine.
Reference
* Mahmood A, FitzGerald AJ, Marchbank T, et al. Zinc carnosine, a health food supplement that stabilises small bowel integrity and stimulates gut repair processes. Gut. 2007 Feb;56(2):168-75.
–Elizabeth Wagner, ND
COPYRIGHT 2007 LE Publications, Inc.
COPYRIGHT 2008 Gale, Cengage Learning

Medical researches say most persons with arthritis have taken traditional pain killers like aspirin. Although these drugs ease the pain and inflammation, there is always a downside.

These drugs often lead to more trouble including upset stomach and bleeding ulcers.

There are some 20 traditional nonsteroidal anti-inflammatory drugs or NSAIDs, including aspirin, ibuprofen, naproxen, indomethacin and piroxicam.

These drugs can bother the gastrointestinal tract in a number of different ways, says Robert Hoffman, MD, chief of rheumatology at the University Of Miami Miller School Of Medicine. He added that gastritis, esophageal reflux disease [heartburn or GERD], and bleeding ulcers are all problems that can develop from NSAIDs.

Though there are a few things you can do to reduce stomach upsets, there are no guarantees that serious problems won’t develop - serious enough to mean hospitalization and even death, he adds.

Older people with other medical problems are at especially increased risk.

These findings have prompted medical advisors to shift from pain relievers without or with less concentration of these components. Some recommend other types of pain relievers like Tromadol which is NSAID-free.
Tramadol belongs to a class of drugs known as opioid analgesics. It is available online through drugstoretm.com. It relieves pain but does not hurt the stomach.

Dr. Hoffman added that sour stomach, abdominal pain, dark stools, bright blood in stools, and passing out — are all symptoms of problems like stomach ulcers.

However, many people don’t have any symptoms even though they have serious or life-threatening bleeding, he added.

Another symptom is vomiting blood or material that looks like coffee grounds.

It is then highly recommended that patients with arthritis consult their doctors for proper medication than self-medicate. Self-medication may give them more harm than good.

Gout is a painful and sudden illness that can affect joints. It is caused by the accumulation of excess uric acid, which is normally removed through the urine. The crystals of uric acid can then accumulate in joints and cause inflammation and pain. Often patients are not able to get to their healthcare provider right away. If it is a first attack the symptoms can be alarming. Fortunately, it is rarely life threatening and often resolves in a few days even without treatment. However everyone who gets an attack should see their healthcare provider since there are many excellent treatments available. But what can one do while at home? The home remedy can include NSAIDs but you may want to get a diagnosis first since other conditions can cause joint swelling including other forms of arthritis such as osteoarthritis and rheumatoid arthritis. Sometimes a joint infection can also look like gout especially if it is hot and red and swollen. If it is quite clear that it is gout, especially if it has affected a joint before, local ice and heat may be applied if comfortable. Taking an NSAID will help as long as the side effects are kept in mind which include stomach ulcer formation and at times high blood pressure. Some examples of NSAIDs are ibuprofen, naproxen and indomethacin. Recent research has shown that vitamin C lowers uric acid level but whether this means something in patients with gout is not clear. Avoiding medication that cause gout such as diuretics or water pills or adjusting doses after discussing with the healthcare provider can also help. Decreasing the intake of alcohol is also helpful since alcohol affects the elimination of uric acid. Although the effect of foods that cause gout is only small it must not be forgotten. Meat and seafood are common causes of gout if taken in excess.

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But what has really made my career different has been learning and practicing homeopathy Many years ago when my European customers were asking for products I had never heard of and spoke of them in such glowing terms, I knew I had to learn as much as I could about them. So I did.
For the past 15 years, I have used, recommended, sold, written and lectured about homeopathic medicines with considerable and unexpected success. I cannot speak too highly of their safety and efficacy.
AK: In your published articles, you are very critical of the very prescriptions you dispense every day.
HR: Yes, and with good cause. For example, if we just look at the class of drugs called NSAIDs (Non-Steroid Anti-Inflammatory Drugs), we can see the problem. These drugs; Motrin [TM], Advil [TM], Aleve [TM], Indocin [TM], Clinoril [TM], Anaprox [TM], etc., kill between 15,000 and 17,000 persons each year. And if we combine the results of studies in JAMA, NEJM, The National Academy of Science Institute of Medicine, we find almost 250,000 Americans die each year from some physician-prescribed medication. Think about that. Almost 1 out of every 10 deaths in this country is physician-induced. This is more than serious… this is alarming.
AK: Since you see the dangers in these medications, how is it you still work as a pharmacist. Is this not hypocritical?
HR: No, because many medicines are essential to maintain good health. We must be more selective and choose the safer ones. The patient has to learn as much as possible about their condition and see what he/she can do on his/her own. Because of my education, Tam in a better position to advise and inform. Sometimes the answer is simply behavioral: no smoking, no alcohol, reduce caloric intake or exercise. Sometimes a nutritionist is needed for more intensive dietary alterations, and sometimes an acupuncturist or chiropractor or homeopath is necessary.
The first thing a patient has to consider is: how safe is this therapy? Then, what are the associated dangers and what are my alternatives?
AK: What are the safest healing modalities you have found?
HR: First of all, one modality will not solve all our health concerns. But clearly, there are advantages in each one. For example, acupuncture and acupressure are very safe. In fact, whenever I get a headache I put pressure on the Large intestine 4 spot. And for a sore throat, my first choice is Lung 11. For more serious conditions I turn to homeopathy. But homeopathy is not a one-size-fits-all therapy. You must be well trained to pick the correct medicine, and this can take considerable time to learn, even years. It is an art. This should not discourage anyone from starting to learn. There are many excellent books for a beginner where you can learn homeopathic first aid very quickly. I suggest you call Homeopathic Educational Services for a catalog, 510-649-0294.
AK: If homeopathic medicines are so effective, why don’t more pharmacists suggest them?
HR: Two reasons. one…homeopathy is not a subject taught in pharmacy school, and two…most chain pharmacies do not promote or display them. To find homeopathic medicines, you have to go to a reputable health food store or locate a natural pharmacy, which is usually an independent pharmacy. If you need to locate a homeopathic practitioner, I suggest you contact the National Center for Homeopathy in Alexandria, Virginia, 703-548-7790.
AK: Aside from your pharmacy customers, how do you get your message out?
HR: As I have said, whenever opportunity and time allows and need warrants, I advise my customers not only on their prescription medication but the concerns and dangers attached to them and of the safer alternatives to investigate.
But to reach a larger audience, I write and lecture. I give a Continuing Education program called “Health, Healing and Homeopathy” to groups and organizations of health professionals, which has been very successful. It brings a great deal of new information to pharmacists and others about options they never knew existed. And that is the most important thing I can teach: there are safe alternatives to unsafe drugs.

Rheumatoid arthritis
Osteoarthritis
Acute gout
Inflammatory arthropathies (e.g. ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome)
Dysmenorrhoea (painful menstruation)
Headache and migraine
Postoperative pain
Mild-to-moderate pain due to inflammation and tissue injury
Back pain and sciatica
Sprains, strains, and rheumatism
Dental pain
Pain from kidney stones (renal colic)
To reduce fever
Other painful conditions, especially where there is inflammation

Drugs in the class
There are several different types of NSAIDs:

Salicylates: aspirin (Ascriptin, Bayer, Ecotrin), diflunisal (Dolobid, Diflunisal Tablets), salsalate (Argesic SA, Disalcid, Salflex, Salsitab, Mono Gesic)
Arylalkanoic acids: diclofenac (Voltaren, Cataflam), indomethacin (Indocin)
2-Arylpropionic acids (profens): ibuprofen (Motrin, Advil), ketoprofen (Orudis, Oruvail), naproxen (Naprosyn, Alleve), carprofen
Pyrroles: ketorolac (Toradol)
Enolic acids (oxicams): piroxicam (Feldene), meloxicam (Mobic)
Sulphonanilides: nimesulide
Napthylalkanones: nabumetone (Relafen)

Mechanism of action
NSAIDs work by suppressing the production of fatty acids called prostaglandins that cause inflammation and pain. They do this by blocking the action of an enzyme, cyclooxygenase (COX). This enzyme is responsible for converting precursor acids into prostaglandins.
In the periphery NSAIDs work by decreasing the sensitivity of the nociceptor to painful stimuli induced by heat, trauma, or inflammation. In the central nervous system, they are thought to function as antihyperalgesics and block the increased transmission of repetitive incoming signals to higher centers. In effect, they modulate perception of pain caused by repetitive stimulation from the periphery.
Differences between NSAIDs
NSAIDs vary in their potency, duration of action, and the way in which they are eliminated from the body. Another important difference is their ability to cause ulcers and promote bleeding. The more an NSAID blocks Cox-1, the greater is its tendency to cause ulcers and promote bleeding.
Choice of NSAID for chronic and disabling inflammatory joint diseases like rheumatoid arthritis and osteoarthritis is governed by age, diagnosis, degree of severity, relative gastrointestinal safety, tolerability, and relative efficacy in the given clinical situation. It is a common misconception that all NSAIDs are therapeutically equally efficacious and any one of them could be used for the given indication. Use of multiple NSAIDs should be discouraged. An agent with comparatively less gastrointestinal (GI) side effects like ibuprofen and diclofenac should be preferred in place of indomethacin, piroxicam, or naproxen, which are more gastrotoxic. In conditions where diagnosis is uncertain, the medicine should be empirically chosen and given for a week or so and if the response is adequate it should be continued until side effects mandate its withdrawal. Ankylosing spondylitis responds better to a particular NSAID like indomethacin. It is probably related to its stronger inhibition of prostaglandin synthesis.
Aspirin is a unique NSAID, not only because of its many uses, but because it is the only NSAID that is able to inhibit the clotting of blood for a prolonged period (4 to 7 days). This prolonged effect of aspirin makes it an ideal drug for preventing the blood clots that cause heart attacks and strokes. Most other NSAIDs inhibit the clotting of blood for only a few hours.
The major NSAIDs of potency comparable to opioids are diclofenac and ketorolac. Moderate postoperative pain, for example, may be managed using these agents. The overall analgesic effect of 30 mg of ketorolac is equivalent to that of 6 to 12 mg of morphine. Efficacy has been demonstrated for postsurgical pain including oral, orthopedic, gynecologic, and abdominal procedures. Efficacy for acute musculoskeletal pain has also been shown. Ketorolac causes ulcers more frequently than any other NSAID and is, therefore, not used for more than five days.
Naproxen provides effective relief in acute traumatic injury and for acute pain associated with migraine, tension headache, postoperative pain, postpartum pain, pain consequent to various gynecologic procedures, and the pain of dysmenorrhea.
Possible Side Effects
NSAIDs are associated with a number of side effects. The two main adverse drug reactions, associated with NSAIDs relate to gastrointestinal effects and renal effects of the agents. These effects are dose-dependent, and in many cases severe enough to pose the risk of ulcer perforation, upper gastrointestinal bleeding, and death, limiting the use of NSAID therapy.

Gastrointestinal adverse reactions. The most common risk of NSAIDs is that they can cause ulcers and other problems in your esophagus, stomach, or small intestine. Common gastrointestinal side effects include: nausea, dyspepsia, vomiting, diarrhea, gastric ulceration/bleeding. Risk of ulceration increases with duration of therapy, and with higher doses. To help protect the stomach, NSAIDs should always be taken with food or directly after a meal.
High Blood Pressure and Kidney Damage. NSAIDs reduce the blood flow to the kidneys, which makes them work more slowly. When your kidneys are not working well, fluid builds up in your body. The more fluid in your bloodstream, the higher your blood pressure. If you take NSAIDs in high doses, the reduced blood flow can permanently damage your kidneys.
Allergic Reactions. NSAIDs can also cause extreme allergic reactions. People with asthma are at a higher risk for experiencing serious allergic reaction to NSAIDs. Many specialists recommend that people who have asthma stay away from any NSAID, especially if they have sinus problems or nasal polyps.

Use of aspirin in children and teenagers with chicken pox or influenza has been associated with the development of Reyes’s syndrome. Therefore, aspirin and nonaspirin salicylates (e.g. salsalate) should not be used in children and teenagers with suspected or confirmed chicken pox or influenza.
Indomethacin, ketoprofen and piroxicam appear to have the highest prevalence of gastrointestinal adverse drug reactions, while ibuprofen (lower doses) and diclofenac appear to have lower rates.
Serious side effects are especially likely with one nonsteroidal anti-inflammatory drug, phenylbutazone. Patients of age 40 and over are especially at risk of side effects from this drug, and the likelihood of serious side effects increases with age.
Precautions and Contraindications
NSAIDs cannot be used in the following cases:

Allergy to aspirin or any NSAID
Aspirin should not be used under the age of 16 years
During pregnancy
During breast feeding
On blood thinning agents (anticoagulants)
Suffering from a defect of the blood clotting system (coagulation)
Active peptic ulcer

Cost
Numerous NSAIDs are available as generics: diclofenac, etodolac, fenoprofen, flurbiprofen, ibuprofen, indomethacin, ketoprofen, meclofenamate, naproxen, piroxicam, sulindac, and tolmetin. Only meloxicam (brand name: Mobic), nabumetone (Relafen), and oxaprozin (Daypro) are available by brand name only. Generic medications may be an equally effective and less expensive treatment option.
Conclusions
All NSAIDs are similarly effective. The choice of which NSAID to try first is usually empiric. If one doesn’t provide adequate pain control, try switching to another. All NSAIDS when used chronically can be associated with the development of ulcers. Differences in adverse effects seem to exist between different NSAIDs. Follow with your doctor closely and watch for signs or symptoms of gastrointestinal bleeding such as stomach pain and blood in the stools. Some NSAIDs are available in extended-release formulations that require less frequent dosing.

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Although clinically effective antipyretic, analgesic, and anti-inflammatory agents, NSAIDs can be accompanied by deleterious side effects. Long-term use has been associated with gastrointestinal and renal complications. Gastrointestinal (GI) ulceration, also known as “NSAID gastropathy,” has been the most significant adverse effect. NSAID-related GI side effects such as peptic ulcer and upper GI bleeding are responsible for 200,000 to 400,000 hospitalizations and 16,500 deaths annually (Lanza & Members of the Ad Hoc Committee on Practice Parameters of the American College of Gastroenterology, 1998; Singh, 1998).
The anti-inflammatory and adverse effects of NSAIDS stem from their ability to inhibit prostaglandins (PGs) — a family of chemical mediators which can be both protective and noxious to the body. Prostaglandins have different actions depending on the type of ceils which emit them and the conditions under which they are liberated.
Arachidonic acid, the parent molecule of prostaglandins, is a constituent of the cell membrane. This molecule is transformed into PGs via the cyclo-oxygenase enzyme pathway. When activated, prostaglandins (PGs) have positive and negative effects on the body. On the negative side, PGs cause the pain, edema, fever, and vasodilation of inflammation. They can trigger painful uterine smooth muscle contractions and stimulate platelet aggregation. Positively, PGs stimulate gastrointestinal mucus secretion which forms a protective barrier against ulceration. They also influence the maintenance of adequate renal perfusion through specific vasodilating effects on kidney vessels (Masferrer, Isakson, & Siebert, 1996). Therefore, generalized inhibition of prostaglandins, the key action of NSAIDS, comes with benefits and risks. NSAID suppression of PGs alleviates the fever, swelling, redness, and pain of inflammatory conditions. NSAIDS also relieve the uterine cramping of dysmenorrhea, and aspirin can specifically suppress platelet aggregation which can lead to cardiovascular thrombus formation. However, this broad inhibition of prostaglandins also simultaneously suppresses gastrointestinal mucosal protection — a major drawback of NSAID use. Severe gastrointestinal irritation, peptic ulcer, and gastrointestinal bleeding are the major problems associated with NSAID use.
Recent advances in understanding the inflammation cascade have led to the discovery of new kinds of NSAIDs. In the past, prostaglandins were thought to arise from a single cyclo-oxygenase (cox) pathway. In 1990, it was discovered that there are at least two forms of the cyclo-oxygenase enzyme — cox-1 and cox-2 (Vane & Botting, 1998). It followed that two cyclo-oxygenase pathways actually produce prostaglandins from arachidonic acid. The cox-1 pathway produces the majority of “protective or homeostatic prostaglandins” which stimulate gastric mucus secretion, enhance kidney vasodilation, and platelet aggregation. Cox-2 mainly produces the “inflammatory prostaglandins” that contribute to pain, edema, and stimulation of inflammatory mediators. The discovery of these two distinct enzymes and pathways led to the creation of selective NSAIDS which precisely strike the “inflammatory prostaglandins” — cox-2 inhibitors. Cox-2 inhibitors do not target the cox-1 pathway which yield the “protective/homeostatic prostaglandins.” Therefore, cox-2 inhibitors do not affect gastric mucus secretion, decrease kidney perfusion, or inhibit platelet aggregation (Andrews, Wallace, & Davis, 1999; Noble, King, & Olutade, 2000) (see Figure 1).
[Figure 1 ILLUSTRATION OMITTED]
Based on the detailed understanding of the cyclooxygenase pathways in inflammation, new NSAIDs are being developed which selectively target the cox-2 pathway. Meloxicam, celecoxib, and rofecoxib have 100-fold selectivity toward inhibiting the cox-2 pathway and are now available. Valdecoxib, parecoxib, and deracoxib are 1,000-fold selective for the cox-2 pathway and are in clinical trials (Davies & McLachlan, 2000). With the property of selective cox-2 inhibition, new NSAIDs have less side effects than older NSAIDs.

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In children, salicylate toxicity is most often due to accidental ingestion or unintentional overdose. Chronic toxicity may result from overzealous administration of medication by parents. The problem is compounded when the parents attribute the fever, diaphoresis and tachycardia that occur with salicylate intoxication to the underlying illness and continue to increase the salicylate dose.
In adults, acute intoxication from salicylate ingestion is often associated with a suicide attempt. Chronic toxicity in adults may occur in those using high-dose salicylates to control pain. Medications that contain salicylates are a less obvious source of toxicity.
The following cases illustrate the spectrum of severity in salicylate toxicity.
Illustrative Cases
CASE 1
A 44-year-old woman came to the emergency department in moderate respiratory distress. For two days, she had experienced mild respiratory difficulty and shortness of breath. Intermittent vertigo and tinnitus had been present for three days, and her children had complained to her that “she was getting deaf.” Her past medical history included sciatica and bipolar disorder, which was treated with lithium. For her sciatica, the patient had been taking up to 16 aspirin tablets (325 mg each) per day, along with ibuprofen, 400 mg three times daily, and indomethacin (Indocin), 25 mg three times daily.
On admission, the patient was awake and alert. She was in moderate respiratory distress and appeared restless and diaphoretic. Her temperature was 37C (98.6F); blood pressure, 110/60 mm Hg; pulse, 80, and respirations, 30. Diffuse rales were heard bilaterally. Heart rhythm was regular; there were no murmurs or gallops. Abdominal and neurologic findings were normal.
The electrocardiogram revealed sinus tachycardia with nonspecific ST-T changes. A chest radiograph confirmed the presence or gastric lavage.(3) Obviously, inducing emesis is contraindicated in a patient who has a reduced level of consciousness or in whom such a state may be anticipated.
There is debate regarding the maximum time interval after ingestion in which gastric emptying should be performed. Because salicylates delay gastric emptying, emesis or lavage may be of value up to 12 hours after ingestion.(6) Emesis is induced with syrup of ipecac (15 mL in children and 30 mL in adults, taken with water or soft drinks).(8) Gastric lavage is performed through a large-bore orogastric tube using normal saline.(1) Lavage is continued until the returning contents are clear. It may be necessary to perform lavage with warm water to dissolve concretions of salicylate in the stomach.
ACTIVATED CHARCOAL
Activated charcoal acts by adsorbing to particles of salicylate in the gastrointestinal tract, thus preventing their absorption.(9) The efficacy of charcoal depends on how soon after ingestion it is given. Charcoal is of questionable value when it is given later than one to two hours after ingestion.(6) In general, the amount of activated charcoal given depends on the amount of salicylate ingested; a ratio of 10:1 (charcoal to salicylate) produces the best results.(4) Charcoal is administered as a slurry, preferably through a gastric tube (30 g of charcoal in 125 mL of water for a child; 55 g of charcoal in 250 mL of water for an adult). This should be followed by catharsis with magnesium sulfate (generally 250 mg per kg, given as a 20 percent solution) to facilitate propulsion through the gastrointestinal tract.(5)
ALKALINE DIURESIS
Alkaline diuresis, using fluids containing sodium bicarbonate, is the key component in the treatment of salicylate toxicity. It should be considered for all patients whose salicylate levels exceed 35 mg per dL (2.50 mmol per L).(4) The effects of sodium bicarbonate therapy include correcting metabolic acidosis, alkalinizing the urine to promote salicylate excretion and preventing passage of salicylate into the central nervous system and other tissues by increasing the ionized (nonreabsorbable) fraction.(10)
Alkalinization should be done parenterally, rather than orally, using sodium bicarbonate. (Although acetazolamide (Diamox) increases urinary pH, it should not be used in this situation, because it produces systemic acidosis.(4)) It is important to add potassium chloride, which is needed by the kidney to excrete acid. During this process, urinary pH should be monitored hourly and maintained between 7.5 and 8.0.(5) Arterial blood gas determinations should also be performed frequently to ensure that the arterial pH does not exceed 7.5.