Steroids - Stress Dose
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ALTHOUGH THE QUESTION is controversial, I still recommend perioperative steroid coverage for patients who are receiving more than 5 mg/day of prednisone or an equivalent and for patients who have recently stopped long-term steroid therapy. The stress dose should be proportionate to the severity of surgical stress and should be given for no longer than 1 to 3 days perioperatively.
Traditionally, patients on long-term corticosteroid therapy are given a brief dosage boost in situations that cause acute physiologic stress, such as surgery, trauma, infection, or severe illness. Although the need for such "steroid coverage" or "stress dosing" has recently been questioned, it seems prudent to continue it for the present.
Unfortunately, stress dosing in patients on long-term corticosteroid therapy has never been studied in large, randomized trials, and some observational studies and small trials suggest that it may be unnecessary. In this situation of uncertainty, clinicians should weigh the physiologic and clinical evidence about the normal hormonal response to surgery, the response in steroid-treated patients, and the risks of adrenal insufficiency.
THE CASE FOR STEROID COVERAGE
The physiologic rationale for steroid coverage is that long-term corticosteroid therapy for chronic autoimmune or inflammatory diseases (such as rheumatoid arthritis, ulcerative colitis, or asthma) suppresses the hypothalamic-pituitary-adrenal (HPA) axis. In normal patients, severe illness, trauma, stress, and surgery are accompanied by activation of the HPA axis. Patients with HPA axis suppression from long-term corticosteroid therapy may be unable to produce this physiologic response to stress.
In normal subjects, daily cortisol production is estimated to be equivalent to 10 to 12 mg of oral hydrocortisone per day.1 Endogenous cortisol levels rise rapidly in response to surgery: cortisol production rises to about 50 mg/day in response to minor surgery, and 75 to 150 mg/day in response to major surgery. This increased production is not uniform: the main increase takes place immediately after anesthesia is induced. Cortisol levels generally return to baseline within 24 to 48 hours after surgery. This short-term elevation of endogenous cortisol has a number of anti-inflammatory and other protective effects that prevent stress-induced hypotension and shock.
The current practice of giving preoperative steroid coverage started when two case reports published in the 1950s described young patients receiving long-term glucocorticoid therapy who died unexpectedly after routine orthopedic surgery.2,3 Their deaths were attributed to adrenal insufficiency, although there was no biochemical confirmation of this.
THE CASE AGAINST STEROID COVERAGE
Recent studies have cast doubt upon this empiric standard of care by questioning not only the dosages but also the necessity of steroid coverage at all.4-6 The question is complicated by poor correlation between biochemical data and clinical outcome.
Is adrenal insufficiency in patients
on corticosteroids clinically important?
Many authors have challenged the need for steroid coverage, pointing out that adrenal insufficiency was confirmed biochemically in only a handful of the reported cases of perioperative hypotension and death that were attributed to secondary adrenal insufficiency. They also point out that many patients on long-term glucocorticoid therapy have undergone major surgery without stress dosing-in some cases, without any steroid therapy at all-and most had uneventful courses.4-8
In 1991, Bromberg et al4 prospectively studied 40 renal allograft recipients admitted to the hospital with significant physiologic stress from sepsis, metabolic abnormalities, or impending surgery. Although baseline prednisone doses were not changed (5-10 mg/day), none of the patients developed clinical adrenal insufficiency. Nevertheless, cosyntropin stimulation test results were abnormal in 25 patients (63%), indicating that biochemical test results do not correlate well with clinical events.
Friedman et al5 prospectively studied 28 glucocorticoid-treated patients who received no dosage boost before a total of 35 major orthopedic operations. The patients had been taking 1 to 20 mg of prednisone for 6 months to 32 years. None of the patients had episodes of clinical adrenal insufficiency, and 18 of the 19 patients with complete data had appropriate biochemical responses to stress.
A randomized, double-blind, placebo-controlled study of 17 surgical patients with biochemical evidence of secondary adrenal insufficiency found that they did not develop signs of adrenal insufficiency when given only their daily dose of steroids.6 The type of surgery ranged from bilateral orchiectomy under local anesthesia to splenectomy under general anesthesia. Unfortunately, the small number of patients was a major limitation of this study.
Hypothalamic-pituitary-adrenal axis
suppression is difficult to predict
Decreased adrenal reserve, as measured by a diminished response to exogenous adrenocorticotropic hormone (ACTH), does not directly translate into clinical adrenal insufficiency. Patients who have received very high doses of corticosteroids are more likely to have decreased response to exogenous ACTH than patients who have received extremely low doses. However, these biochemical test results are poorly correlated with clinically apparent adverse effects.
In addition, recent research shows that even this biochemical HPA suppression cannot be accurately predicted from the traditional risk factors: duration of corticosteroid therapy, highest dose of corticosteroid, and total cumulative dose. In a large study of patients receiving daily long-term therapy with 5 to 30 mg of prednisone or an equivalent, Schlaghecke et al9 found that pituitary-adrenal function could not be reliably predicted by the dose or duration of glucocorticoid therapy. In another study of patients on doses of up to 10 mg/day, none of the patients receiving less than 5 mg had a suppressed HPA axis, and the remaining patients had widely varied responses.10 Suppression could not be predicted by the total dose, the highest dose, or the duration of therapy.
Furthermore, the time to HPA axis recovery after stopping glucocorticoids may vary. It has been reported to be as little as 2 to 5 days and as long as 9 to 12 months.11
Thus, it is difficult to predict the presence of HPA axis suppression from the patient's history of corticosteroid use.
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There is overwhelming evidence which shows that creatine supplementation does cause an increase in the amount of creatine phosphate in muscles. Harris et al (1992) conducted a study examining creatine content in the quadriceps femoris muscle in 17 subjects after supplementation of 5 g of creative monohydrate 4-6 times a day for two days. The results found a significant increase in the total creatine level in all subjects but the results were especially noticeable in those with the lowest muscle creatine store at the start of the study. To determine whether exercise could affect the amount of creatine absorbed by muscles, some of the participants followed a unique training program. During supplementation, they pedaled a bicycle ergometer for one hour each day while using only one leg to supply the pedaling force. With supplementation, the unexercised legs increased their creatine levels by about 25 percent, but the exercised legs increased their creatine levels by 37 percent. It is hypothesized that exercise increases the flow of blood to the muscles or changes the rate at which muscles absorb creative from the blood, thus improving the creatine loading effect. Another study conducted by Febbraio replicated the results obtained by Harris.
Several studies also show that creatine supplementation does cause an increase in muscle strength. Earnest et al (1995) conducted a study investigating the influence of creatine monohydrate supplementation on muscular power and strength in 10 experienced weight trained male subjects. Three series of high intensity, anaerobic type muscular workouts were used. The first series consisted of three consecutive 30 second Wingate bike tests, followed by five minuets of rest. Peak anaerobic power was defined as the greatest power achieved in a given five second work interval. Anaerobic work was defined as the total amount of work performed in a 30 second period. The second series used a one repetition maximum (lRM) free weight bench press as a test of muscular strength. The third series utilized complete lifting repetitions at 70% of the bench press IRM until fatigue. Fatigue was defined as the inability to complete one lifting repetition or the inability to maintain a lifting cadence of one second eccentric and one second concentric (lifting and lowering the weight). Total lifting volume was calculated as 70% of pre-test IRM multiplied by the number of complete lifting repetitions. Subjects received either a glucose placebo or creatine monohydrate supplement in a double blind fashion. (After 14 days of supplementation, each subject was re-tested on the Wingate bike tests. Re-testing for the weight lifting trials was done after 28 days of supplementation.
Within the creatine group, total anaerobic work from the Wingate tests was significantly higher during all post-test trials. The increases were 13% for series one, 18% for series two and 18% for series three. No changes were noted in the placebo group. Greater total anaerobic work resulted from the creatine subject's ability to achieve and maintain higher levels of anaerobic power consistently over- each five second time interval. Bench press IRM increased 6% in the creatine group. Total lifting volume was significantly higher within the creatine group, whether expressed in absolute terms (26%) or relative terms (29%). Increases in the total lifting volume were associated with the ability of the creatine group to perform 26% more lifting repetitions. The authors conclude that the ability of the creatine group to perform a greater total lifting volume demonstrates the effectiveness of creatine as an ergogenic aid.
In Hultman's study (cited in Anderson, 1974) these results were replicated. Each day, creatine was given in six separate doses of five grams a day. During the six-day period, five other Estonian runners of comparable ability received a glucose placebo instead. All runners were unaware of the actual composition of their supplements. Before and after the six-day supplementation, the athletes ran four 300-meter and (on a separate day) four 1000-meter intervals, with three minutes of rest between the 300-meter intervals and four minutes of rest between the 1000-meter intervals. Improvement on the final 300-meter interval (from pre-to-post supplementation) was more than twice as great for creatine users, and improvement was more than three times as great for creatine supplements in the final 1000-meter interval. Total time to run all four 1000-meter intervals improved from 770 to 757 seconds after creatine supplementation. In comparison, the placebo group actually slowed from 774 to 775 seconds.
In Hultman's study (cited by Anderson, 1994) creatine supplementation was very important during the last interval of each workout. Creatine supplementers doubled their advantage during the final 300-meter interval and tripled their advantage in the closing 1000-meter sprint. This supports Hultman's hypothesis that creatine is likely to be most helpful when lactic acid levels are highest and fatigue is greatest. Hultman thus feels that creatine serves as a buffer lowering lactic acid muscle burn and delaying fatigue, thus allowing an athlete to perform longer workouts.
In contrast, Balsom at al (1993) investigated the influence of creatine supplementation on endurance exercise performance in the form of a 6 km run and showed that creatine supplementation does not enhance performance or increase peak oxygen uptake during prolonged continuous exercise. There was actually decreased performance in the creatine supplementation group, which may be attributed to the participants weight gain.
In support of Balsam et al (1993), Febbraio et al (1995) conclude that creatine supplementation "may not increase performance during exercise where a significant proportion of energy is derived form aerobic metabolism." This aerobic metabolism occurs during more prolonged, sustained exercise as opposed to anaerobic metabolism which occurs during fast, nonsustained muscle contractions. It is therefore more likely that if creatine supplementation has an effect it will only be seen during brief, anaerobic exercise such as sprinting or weight lifting.
As you may or may not know, creatine monohydrate will not fully dissolve in liquid. That's why you always get that gritty sand at the bottom of the glass. Look at it this way, if it falls like sand to the bottom of your glass what does it do in your stomach? Maybe that explains why so many complain of stomach discomfort when using regular creatine monohydrate.
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Creatine works by enhancing muscle cell hydration. It is very important to consume adequate fluids while taking creatine to see best results. A good rule of thumb is to drink an EXTRA 16 to 20 ounces of liquid for every 5 grams of creatine you take.
During your Loading Phase you should be drinking an EXTRA 64 to 80 ounces of liquid than you normally drink. During the maintenance phase you should drink an EXTRA 32 to 40 ounces.
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