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21/ AMS <* THIS PANEL *> 22/ Babies and Kids 23/ A bit of song (like camp songs) 24/ What is natural? 25/ A romantic notion of high-tech employment 26/ Other news groups of related interest, networking 27/ Films/cinema references 28/ References (written) 1/ DISCLAIMER 2/ Ethics 3/ Learning I 4/ learning II (lists, "Ten Essentials," Chouinard comments) 5/ Summary of past topics 6/ Non-wisdom: fire-arms topic circular discussion 7/ Phone / address lists 8/ Fletcher's Law of Inverse Appreciation / Rachel Carson / Foreman and Hayduke 9/ Water Filter wisdom 10/ Volunteer Work 11/ Snake bite 12/ Netiquette 13/ Questions on conditions and travel 14/ Dedication to Aldo Leopold 15/ Leopold's lot. 16/ Morbid backcountry 17/ Information about bears 18/ Poison ivy, frequently ask, under question 19/ Lyme disease, frequently ask, under question 20/ "Telling questions" backcountry Turing test (under construction) AMS (acute mountain sickness) -- UNDER CONSTRUCTION A recurring topic of discussion is altitude sickness and treatment. AMS (acute mountain sickness) Time and a distinct lack of resources can quickly elevate the dangers of a medical emergency. High Altitude Pulmonary Edema (HAPE), High Altitude Cerebral Edema (HACE), and retinal hemorrhaging are all problems which can take place in some individuals as low as 5-8,000 feet. You can read references, but you have a responsibility to be in reasonable physical shape, drinking plenty of fluids. But the important thing to realize is that you have a MARGIN of safety that you are cutting. You should consult YOUR physician about YOUR special needs. Diamox or Previtin should not be taken lightly. [Do you understand the concept of body/drug interactions?] Reactions to other drugs (even aspirin), allergries can differ at higher elevations. See a physician. Another topic where urban thinking can harm you. Drug treatment is not a substitute for descending. [Do you understand the concept of body/drug interactions?] Gamow bags have been discussed as an expensive measure (perhaps most useful for high altitude expeditions). Bottled LO2 is also a possibility. The medical definition of what constitutes a high altitude starts at 8,000 ft. This is the elevation where the PO2 is .75 that of a standard atmopshere. 14,000 ft. is .666 (2/3) a ATM, and 18,000 ft. is 1/2 an ATM. This is clearly non-linear [check your linear thinking at the door]. So the problem ranges are: 8,000-14,000 ft. 14,000-18,000 ft. Above 18,000 ft. Bibliography: 1 Ferreira and Grundy, _Dexamethasone in the Treatment of Acute Mountain Sickness_, NEJM, VOl. 312, No 21, page 1390, 23 May 1985. 2 Oelz, Oswald, _A Case of High-Altitude Pulmonary Edema Treated with Nifedipine_, JAMA, Vol 257, No 6, page 780, 13 Feb 1987. "Medicine for Mountaineering: Third Edition" edited by James A. Wilkerson, M.D., 1985, The Mountaineers, ISBN 0-89886-086-5. "Medicine for the Outdoors" by Paul S. Auerbach, M.D., 1986, Little, Brown and Company, ISBN 0-316-05928-5 (hc) 0-316-05929-3 (pbk). "Wilderness Medicine" by William Forgey, M.D., 1987, ICS Books, Inc., ISBN 0-934802-37-8 "Mountain Sickness" by Charles S. Houston Scientific American, October 1992, page 58. Synopsis at top of the article says: "The varied and subtle symptoms of this potentially lethal disorder humble many who scale the summit. But the problem is often preventable." Jim West's book. "NOLS Wilderness First Aid" by Tod Schimelpfenig and Linda Lindsey, 1991, National Outdoor Leadership School and Stackpole Books, ISBN 0-8117-3084-0 %X Just finished the book. Excellent. Too repetitive at some points is my only real criticism. Excerpt from the Physician's Desk Reference, 1993 Diamox is a potent carbonic anhydrase inhibitor, effective in the control of fluid secretion (e.g. some types of glaucoma), in the treatment of certain convulsive disorders (e.g. epilepsy), and in the promotion of diuresis in instances of abnormal fluid retention (e.g. cardiac edema). Diamox is an enzyme inhibitor that acts specifically on ... the hydration of carbon dioxide and the dehydration of carbonic acid. In the eye, this inhibitory action decreases the secretion of aqueous humor and results in a drop in intraocular pressure, a reaction considered desirable in cases of claucoma. ... The diuretic effect of Diamox is due to its action in the kidney on the reversible reaction involving hydration of carbon dioxide and dehydration of carbonic acid. The result is renal loss of HCO3 ion, which carries out sodium, water, and potassium. Diamox Sequels sustained-release capsules provide prolonged action to inhibit aqueous humor secretion for 18 to 24 hours after each dose, whereas tablets act for only 8 to 12 hours. ... Blood concentrations of Diamox peak between 3 to 6 hours after administration of Sequels, compared to 1 to 4 hours with tablets. Placebo-controlled clinical trials have shown that prophylactic administration of Diamox at a dose of 250mg every 8 to 12 hours (or 500mg Sequels once daily) before and during rapid ascent to altitude results in fewer and/or less severe symptoms (such as headache, nausea, shortness of breath, dizziness, drowsiness, and fatigue) of acute mountain sickness (AMS). Pulmonary function is greater in the Diamox treated group, both in subjects with AMS and asymptomatic subjects. The Diamox treated climbers also had less difficulty in sleeping. ... Diamox therapy is contraindicated in situations in which sodium and/or potassium blod serum levels are depressed, in cases of marked kidney and liver disease, in suprarenal gland failure, and in hyperchloremic acidosis. It is contraindicated in patients with cirrhosis because of the risk of development of hepatic encephalopathy. ... Fatalities have occurred, although rarely, due to severe reactions to sulfonamides including Stevens-Johnson syndrome, toxic epidermal necrolysis, fulminant hepatic necrosis, agranulocytosis, aplastic anemia, and other blood dyscrasias. ... Caution is advised for patients receiving concomitant high-dose aspirin and Diamox, as anorexia, tachypnea, lethargy, coma, and death have been reported. Increasing the dose does not increase the diuresis, and may increase the incidence of drowsiness and/or paresthesia. Increasing the dose often results in a decrease in diuresis. ... Gradual ascent is desirable to try to avoid acute mountain sickness. If rapid ascent is undertaken and Diamox is used, it should be noted that such use does not obviate the need for prompt descent if severe forms of high altitude sickness occur, i.e. pulmonary edema or cerebral edema. ... Long term studies in animals to evaluate the carcinogenic potential of Diamox have not been conducted. In a bacterial mutagenicity assay, EE was not mutagenic when evaluated with and without metabolic activation. The drug had no effect on fertility when administered in the diet to male and female rats at a daily intake of up to four times the maximum recommended human dose. Diamox has been shown to produce birth defects of the limbs in mice, rats, hamsters, and rabbits. There are no adequate and well-controlled studies in pregnant women. EE should be used in pregnancy only if the potential benefit justifies the potential risk to the fetus. Because of the potential for serious adverse reactions in nursing infants from EE, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. The safety and effectiveness of Diamox in children have not been established. Adverse reactions, occurring most often early in therapy, include a "tingling" feeling in the extremities, hearing dysfunction or tinnitus, loss of appetite, taste alteration and gastrointestinal disturbances such as nausea, vomiting, diarrhea, and occasional instances of drowsiness and confusion. ... No data are available regarding Diamox overdosage in humans as no cases of acute poisoning with this drug have been reported. Animal data suggest that Diamox is remarkably non-toxic. No specific antidote is known. Treatment should be symptomatic and supportive. Electrolyte imbalance, development of an acidotic state, and central nervous system effects might be expected to occur. ... Dosage is 500mg to 1000mg daily, in divided doses using tablets or Sequels as appropriate. In circumstances of rapid ascent, such as in rescue or military operations, the higher dose level of 1000mg is recommended. It is preferable to initiate dosing 24 to 48 hours before ascent and to continue for 48 hours while at high altitude, or longer as necessary to control symptoms. Store at controlled room temperature (59 to 86 deg F). http://188.8.131.52/hra/brochure.html http://184.108.40.206/hra/AMS-clinguide.html -----tage line----- From: email@example.com (ANDREA FAUSTINA) Newsgroups: rec.skiing.alpine Subject: Re: altitude sickness As written in the PharmAssist: Drug Class & Use: This drug is a Carbonic anhydrase inhibitor used to treat insomnia, fluid retention, glaucoma, epileptic seizures, and shortness of breath. Related Generic Names: Acetazolamide Dichlorphenamide Methazolamide Related Brand Names: Acetazolam Ak-Zol Apo-Acetazolamide Daranide Dazamide Diamox Diamox Sequels Neptazane General Information: Addiction Potential? No Prescription Required? Yes Available in generic form? Yes Decreases fluid retention (and internal eye pressure) by preventing the action of carbonic anhydrase. Time Required To Take Effect: Allow approximately 2 hours for this drug to take effect. What to do if a Dose is Missed: Retake as soon as you remember, then continue based on the original schedule. Possible Adverse Effects: Life threatening can include convulsions. If this occurs contact Emergency Medical Help Immediately. On rare occasion some may experience ringing ears, irregular or weak heartbeat, fever, back pain, headache, hives, nausea, vomiting, blood in urine, mood changes, confusion, hoarseness, trembling, and difficulty breathing. If this occurs cease taking this drug and consult with your doctor as soon as possible. Possible Drug Interactions: 1. May increase the effect of Amphetamines, Tricyclic Antidepressants, Quinidine and Sympathomimetics. 2. May diminish the effect of Aspirin, Lithium and Methenamine. 3. May result in toxicity when used with Digitalis preparations and Salicylates. 4. May increase the loss of potassium when used with oral Antidiabetics, Cortisone drugs and Diuretics. 5. May result in a loss of bone minerals when used with Anticonvulsants. Caution/Alert: 1. This drug should not be used if you have kidney disease, diabetes, adrenal grand failure, or are allergic to any carbonic anhydrase inhibitor. 2. Before using this drug consult with your doctor if you have lupus, gout, are allergic to any Sulfa drug, or will be having surgery (including dental) within the next 2 months requiring either spinal or general anesthesia. 3. If pregnant or breast-feeding consult with your doctor before using this drug. 4. People over 60 years of age should consult with your doctor before using this drug. 5. This drug should not be given to children under 12 years of age. 6. Extended use of this drug may result in jaundice, kidney stones, weight loss, vision changes, and a possible loss of both taste and smell. Overdose Symptoms: Overdose symptoms can include a numbing sensation in the hands and feet, confusion, nausea, vomiting, drowsiness, excitability and coma. If you suspect an overdose contact medical help and area Poison Control Center immediately. Andrea From: firstname.lastname@example.org (Prospero Barquero Gogo) Newsgroups: rec.skiing.alpine Subject: Altitude sickness Date: 2 Nov 1994 18:30:52 -0500 Organization: The George Washington University School of Medicine There is really not much one can do for mountain sickness. In the August Journal of Wilderness Medicine, they reviewed the origins and attempted treatments for altitude sickness. To sum it up: (1) physical fitness has no effect on altitude sickness (although all the test subjects were in relatively good shape); (2) people are unpredictably susceptible to acute mountain sickness (AMS) (3) AMS and the often associated high-altitude pulmonary edema (when water leaks into your lungs; HAPE) happen less often in people who (a) subconsciously increase their breathing (even while asleep) and (b) respond to high altitude (greater than 8000 feet) by concentrating their blood oxygen carrying component (by diuresis -- that is, peeing alot). (4) AMS can be prevented in the short run by taking a diuretic (this is technical but, one of the carbonic annhydrase inhibitor class). It prevents AMS by making you pee, and causes you to breathe more by decreasing the pH of your blood (breathing brings the pH back to normal). (5) the reason one needs to "acclimate" to high altitude is that it takes the body some time to manufacture new red blood cells, which carry oxygen to your tissues, among other physiologic changes. (6) diuretic therapy in the long run is controversial because it decreases the body's response of making new red blood cells. (7) hyperbaric chambers (where one is surrounded by sea level atmosphere pressure) are effective treatments for severe AMS and HAPE As someone has already posted, drinking lots of water is beneficial when going to high altitude. This prevents dehydration, and it also improves your body's chances of responding by diuresis. The diuretic mentioned earlier can only be obtained from your doctor in the USA, and be aware that it may have side effects, as any drug. Usually, take the diuretic only if you've had problems with high altitude before, or if you're going to very high altitudes (>13000 feet). I'll try to answer any other questions if I get them via email. Perky Gogo email@example.com Newsgroups: rec.climbing From: firstname.lastname@example.org (Jim Beall) Subject: RE: AMS and Tums/Rolaids/etc Regarding recent posts wondering about the reputed benefits of taking Tums or Rolaids to reduce the effects of altitude sickness: Here is a brief quote from Peter Hackett, M.D.'s 1984 book "Mountain Sickness: Prevention, Recognition and Treatment" (ISBN 0 930410 10 6) "Aluminum hydroxide sodium carbonate (Roliads) has been suggested as a prophylaxis for acute mountain sickness (Penberthy, 1977). It is incorporated into a four-point prevention program designed for Mt. Rainier climbers which includes: 1) adequate hydration, 2) high carbohydrate intake while climbing, 3) Rolaids to maintain urine pH at 5.5 to 6.5 (slightly acid), and 4) regulating climbing pace to keep the heart rate (pulse) below two-thirds of maximum. It is the opinion of this writer [Dr. Hackett] that such a program on Mount Rainier is of obvious value in preventing acute mountain sickness, even without the use of Rolaids. There has not, as of this writing, been a controlled study on the use of Rolaids and although there are no noted harmful side effects in the dosages recommended, we do not recommend its use as mountain sickness prophylaxis." Granted it's a ten year old reference, but the story's been around for much longer. Another gem from Hackett's little book: "Local Sherpa wisdom dictates never to get drunk the first night at altitude"! From: email@example.com (Tom Bunch) Newsgroups: rec.climbing Subject: Re: altitude sickness FYI Date: 4 Jan 1995 03:39:43 GMT In my original post I omitted the side effects of Diamox. I did this because I didn't really understand how they worked, and I didn't want to spread still more misinformation on the whole topic, but in retrospect, I'm afraid people might assume I've told the whole story. Fortunately, Allen Sanderson (firstname.lastname@example.org) took the time to fill in the blanks for me, and point out one or two other things. I will include the relevant bits of his letter (with permission). Also I remember reading a post here about an alternative drug in testing, but I couldn't remember any specifics. The post turns out to have been by Denzil Boradhurst regarding bnezolomide, and I will append it as well. This info may never, sadly, become useful since, as Denzil points out, it does not seem to have a profitable market and so probably won't be produced. -Tom -- From: Allen Sanderson Diamox is a trademark name for acetazolamide. You are almost correct in what an acetazolamide does. It is an ihibitor, but not quite everywhere you mention in the chemical reation. [I'm sure this is what he meant, but actually it inhibits production of the enzyme that catalyzes the reaction, which amounts to the same thing. -Tom] Bicarbonate reduces down to hydronium and carbonite acid. Carbonic anhydrase comes into play in breaking down the carbonic acid into water and carbon dioxide which is expelled through your renal system (kidneys) and repitory system (lungs), respectively. You kinda implied that cardonic anhydrase helps break down bicarbonate which it does not - it only affects the second reaction. [This contradicts what was told to me by a physician, but Allen may be right -- this physician emphasized that he was not current on this stuff. -Tom] Now when you take acetazolamide it inhibits the break down of carbonic acid into water and carbon dioxide. Thus it makes your blood acidic (ie brings on acidosis) because there is too much carbonic acid in the blood. Your body reacts in two ways. First, it tries to bring in more oxygen so a pH balance is maintianed between oxygen and the carbonic acid which is what we want. But at the same time your body tries to dump the extra carbonic acid (and other good elecrolytes and water that you really want to keep) through the renal system, not what we want. So you end up breathing more, slight hyperventilation, and you piss like a race horse. So as you can see it does help but at a price. -- From: email@example.com (Denzil Broadhurst) Date: Wed, 26 Oct 94 10:14:54 GMT Just returned from the British Medical Expedition to Everest - great time, though I wasn't one of the people climbing Everest, just some of the trekking peaks (20,000-21,000 ft). One of the medical trials was a double blind test on Benzolomide to see if it had the same effects for acclimatisation as Acetazolomide (Diamox). Provisional results show it to be just as effective, and with fewer side effects. You still get the tingles in extremities, (including one area where the ladies wouldn't suffer from!) but it doesn't seem to affect the mental state like Diamox. Now for the bad news! The drug was manufactured in the 60's as a possible replacement for Diamox in treatment of Glaucoma - but it didn't work. No more has been made and we've just used up the world stocks in the trial! Anyone out there working for a drugs company prepared to make some more (and put it through the necessary safety trials - shouldn't cost more than a couple of million!)? The doctor in charge of the trial will be publishing his finding and talking to various Pharmaceutical companies, but if its only application is AMS it is likely that there wouldn't be sufficient demand to justify the investment. Shame really, one of the guys with me had problems 15 years back with AMS when he went to Everest base camp, this time on the trial he got up to 21,000 ft with no problems. From: firstname.lastname@example.org (Tom Bunch) Newsgroups: rec.climbing Subject: Re: altitude sickness FYI Date: 31 Dec 1994 03:09:06 GMT In article <email@example.com>, BillOldMan <firstname.lastname@example.org> wrote: >Just a little more on using tums to avert mild AMS; The hypothsis is that >overbreathing at altitude, from exertion or other causes, results in loss >of CO2, which results in loss of carbonic acid (H2CO3) which normally >causes the acid shift in blood that stimulates nerves in the central >nervous system which stimulate breathing, but the body needs O2 and begins >to compensate for the loss of CO3 by providing CO3 ions from other >sources, and runs low, short term, so tums help balance things out, short >term. Seems as though low carbonic acid should result in alkalosis, and >that adding an antacid should make things worse, but it's the carbonate >ions that are lost and that are replaced by tums. I think dehydration is a >bigger threat, but I've never run into serious problems, being a more or >less a moderate mountaineer. That's the hypothesis, more or less, but it's been been pretty conclusively debunked. Another important part of the theory is that the phenomnae noted above trigger vasodilation in the brain (maybe elsewhere too -- I'm a lay person) which can lead to hypoxic brain damage. I decided it was silly to live with all the misinformation on the Rolaids thing, so I gave Tom Hornbein a buzz, since his office is quite near mine. Dr. Hornbein was interviewed in the most recent in R&I in the article by Alan Fitch. He's one of the foremost researches on all this rot. Any errors this post may (is likely to) contain are mine. Anything particuarly clever is probably his. The skinny is this: the Rolaids idea came from Larry Penberthy, then owner and president of MSR. This was his new idea, after his suggestion of superdoses of the watersoluble vitamins fell from favor. Rob Roach, who was at the time a grad student at Evergreen (here in Washington state) did a controlled study of aluminum hydroxide sodium carbonate versus (Rolaids) on Mt. Rainier and found, as a majority of respectable scientists predicted, no benefit. Hornbein wrote a critique of Penberthy's unconventional interpretation of the scientific method, and Penberthy wrote irate letters to the Dean of the medical school and the President of U. Washington, then Charles Oderguard. The critique was published in one of the climbing rags, maybe _Summit_ or _Climbing_. I wish I could tell you more specifically, but I can't. Doc Hornbein had considered this history more or less successfully repressed until I brought it up. He was openly shocked at the idea that anyone was still recommending Rolaids to stave off AMS. After Larry Penberthy gave up on all this, he made an abortive bid for U.S. Senate, which is, I suppose, totally irrelevant. Now I'm going to go farther out on a limb and try to describe what Diamox is all about. Diamox is a carbonic anhydrase inhibitor. Carbonic anhydrase (henceforth C.A.) is an enzyme carried around mostly by red blood cells which aids carbon-dioxide transport from the tissues and its release from the blood in the lungs by catalyzing the reversible hydration of carbon dioxide to carbonic acid. Vastly simplified, the body produces lots of h2co3 (bicarbonate) when sugars are used, and C.A. is a catalyst as it goes to h+ and hco3- (hydronium ion and carbonic acid) and from there to h20 and c02. Inhibitting C.A. merely slows down this reaction. I'm still a little mystified by the intricacies of it -- intuitively, how can you correct an imbalance by inhibitting the enzyme the body uses to readjust that balance? But my understanding is that hyperventilation causes you to blow off an excess of co2, resulting in acidosis which can lead to cerebral edema. But if co2 is not so readily available to be blown off, it's just retained as carbonic acid or bicarbonate. Apparently, loading up with that dross doesn't inhibit absorbtion of o2. Bicarbonate, by the way, is the most important PH buffering agent in our bodies. Also, bear in mind that some of this stuff is still just theory. For example, it's still debatable that acidosis -> vasoconstriction in the brain -> hypoxic brain damage and cerebral edema. Another thing Dr. Hornbein went into was that inhibitting C.A. raised the difference in partial pressure of CO2 between, I think, arteries and capillaries, which in turn keeps the CO2 out in the tissue instead of in the blood where it will have to be dealt with. My understanding of this last bit is minimal, and I didn't want to keep him busy too long answering dopey questions. Anyway, given all the above, it's not surprising that people might think Rolaids might help -- it's full of carbonate. The fact is, it only helps with indigestion and such. One controlled study (again, I can't cite it specifically) got results something like this with Diamox: incidence of headache patients with nothing 70% patients with placebo 50% patients on Diamox 7% This was on a two day climb of Mt. Rainier (14,410 ft). It's generally accepted that headaches and nausea are at one end of the spectrum that leads to cerebral edema. Whether the mechanisms are approximately the same for pulminary edema is a matter of less concensus. An alternative drug is Decadon (sp?), a steroid. There has been no comparing study between the two so far as Dr. Hornbein knows. I should think, given the prevalence of Diamox, that Decadron is only of interest to patients for whom Diamox is contraindicated, such as those with acute narrow angle glaucoma (rare form of glaucoma). Effectiveness of Diamox has been shown to vary quite significantly between individuals. Basically, you want to ask your doctor about it, but most prescribe 250mg two or three times per day. Many believe that once per day is enough, but once you've found what works, you tend to stick with it. If you take what is, for you, a large dose, you will get tingly sensations in your extremities. If it's not uncomfortable, fine. But it can apparently make you feel "really weird". If so, you should (again, ask the prescribing doctor) be ok to cut your dosage in half. I tried to look up a few specific citations just now, but apparently the database is down. Isn't it great having computers to blame for things? -Tom Bunch P.S. If we're lucky T.H. himself may come around and clarify this further for us -- I pointed him in the general direction of rec.climbing. Now, if he can suffer all the slings and arrows, perhaps we'll see his face here. Article 34948 of rec.climbing: From: email@example.com (Tom Dunwiddie) Subject: Re: Neurological effects of high altitude Well, here's a few to get you started... not complete agreement, but most of them do seem to suggest that there are some problems following climbing at high elevation. Now if they could just figure out what's wrong with our brains to make us climb to begin with. 8^) Tom Dunwiddie ----------- AU - Cavaletti G AU - Tredici G TI - Long-lasting neuropsychological changes after a single high altitude climb. AB - Acute neuropsychological changes due to high altitude climbing without supplementary oxygen are well known. However, many climbers report vague symptoms of brain dysfunction after return to sea level suggesting that long-lasting neuropsychological impairment may ensue even after a single ascent. In this study we evaluated a series of neuropsychological functions in a group of 11 climbers who ascended over 5000 m. Besides memory, also reaction time and concentration were less efficient when the climbers were evaluated 75 days after their return to sea level, confirming that even a single high altitude climb may be harmful for central nervous system functions. SO - Acta Neurol Scand 1993 Feb;87(2):103-5 AU - Regard M AU - Landis T AU - Casey J AU - Maggiorini M AU - Bartsch P AU - Oelz O TI - Cognitive changes at high altitude in healthy climbers and in climbers developing acute mountain sickness. AB - We report the cognitive functions of 17 non-acclimatized mountaineers who ascended from low lands to an altitude of 4,559 m in 24 h and were studied there within 6 h. We found that this rapid ascent to high altitude had small, but differential effects upon cognitive performance depending upon the later development of acute mountain sickness (AMS). Subjects who developed AMS within a 24-48-h stay at high altitude were mildly impaired in short term memory, but improved in conceptual tasks, while subjects who remained healthy had a better short term memory performance but no improvement in cognitive flexibility. Possible explanations for these unexpected effects of high altitude are discussed. SO - Aviat Space Environ Med 1991 Apr;62(4):291-5 AU - White AJ TI - Cognitive impairment of acute mountain sickness and acetazolamide. AB - In a trial to assess the cognitive impairment attributable to benign acute mountain sickness (AMS) and to acetazolamide, six women and five men, 20-35 years old, ascended from sea-level to 3600 m in 36 h and were assessed for deterioration in performance on psychological tests. Of five sex-matched pairs with a mean age difference of 3.4 years (S.D. +/- 4.4 years), one member took slow-release acetazolamide 500 mg daily and one placebo on a double-blind basis during the ascent and again for an identical course at low altitude 32-38 d later. The unmatched woman took placebo during ascent. Before, during, and after each drug course each subject performed an Environmental Symptom Questionnaire (ESQ) and a psychological test battery consisting of trail-making, paced auditory serial addition test (PASAT), letter-digit code, dual-task cancellation and subtraction, and memory subtests. On ascent, ESQ score deteriorated by an average of 62 points in placebo subjects compared with 32 in acetazolamide subjects (p = 0.055). Deterioration in the psychological test battery was only significant in the PASAT (p less than 0.05) and memory (p less than 0.01) subtests of subjects taking placebo. For those taking acetazolamide, no test showed significant impairment, suggesting it had no detectable cognitive impairment at this dose. SO - Aviat Space Environ Med 1984 Jul;55(7):598-603 AU - Jason GW AU - Pajurkova EM AU - Lee RG TI - High-altitude mountaineering and brain function: neuropsychological testing of members of a Mount Everest expedition. AB - Concern has been raised regarding the possibility that hypoxic conditions encountered during high-altitude mountaineering may have lasting harmful effects on the human brain. Members of an expedition to Mount Everest completed a series of neuropsychological tests before and after the expedition. Exposure to altitudes above 7,200 m was limited to a maximum of four consecutive nights, separated by rest periods at lower altitudes. No significant decline in performance was observed on any test. The subjects also completed a short series of tests at different altitudes during the expedition. No significant deterioration was observed at altitudes up to 7,500 m. There do not appear to be lasting harmful effects on brain function under these conditions. SO - Aviat Space Environ Med 1989 Feb;60(2):170-3 AU - Cavaletti G AU - Garavaglia P AU - Arrigoni G AU - Tredici G TI - Persistent memory impairment after high altitude climbing. AB - High altitude climbing without supplementary oxygen is a common sporting practice and athletes have been extensively evaluated with respect to possible brain functional impairment during its performance. Little is known on the contrary about long-term effects of hypoxia on the central nervous system. We evaluated, at sea level, a group of 10 high-altitude climbers with a battery of neuropsychological tests before and 75 days after the ascent. Our results suggest the occurrence of an impairment of memory performance after return to sea-level at least in some subjects, while speech and certain practical abilities were unchanged. SO - Int J Sports Med 1990 Jun;11(3):176-8 AU - Hornbein TF TI - Long term effects of high altitude on brain function. AB - Absence of oxygen to the brain for even a very few minutes results in loss of consciousness and can cause permanent injury. Can the wanderer to the limits of earth-bound hypoxia suffer similar harm from more prolonged exposure to milder hypoxia that does not cause loss of consciousness? I shall review the results from studies where neurobehavioral function has been compared in mountaineers before and after return from great heights and in individuals with chronic pulmonary disease before and after prolonged, continuous oxygen therapy. Many (although not all) of these studies report mild impairment of neurobehavioral function after fairly prolonged hypoxic exposure. Impairment was manifest by deficits in memory storage and recall, aphasia, concentration, and finger tapping speed; the last deficit was still detectable a year later in one group of mountaineers. Limited evidence suggests that climbers with a high ventilatory response to hypoxia (HVR) may be more susceptible to impairment than those with a lower HVR. SO - Int J Sports Med 1992 Oct;13 Suppl 1:S43-5 AU - Hornbein TF AU - Townes BD AU - Schoene RB AU - Sutton JR AU - Houston CS TI - The cost to the central nervous system of climbing to extremely high altitude. AB - To assess the possibility that climbing to extremely high altitude may result in hypoxic injury to the brain, we performed neuropsychological and physiologic testing on 35 mountaineers before and 1 to 30 days after ascent to altitudes between 5488 and 8848 m, and on 6 subjects before and after simulation in an altitude chamber of a 40-day ascent to 8848 m. Neuropsychological testing revealed a decline in visual long-term memory after ascent as compared with before; of 14 visual items of information on the Wechsler Memory Scale, fewer were recalled after ascent by both the simulated-ascent group (a mean [+/- SD] of 10.14 +/- 1.68 items before, as compared with 7.00 +/- 3.35 items after; P less than 0.05) and the mountaineers (12.33 +/- 1.96 as compared with 11.36 +/- 1.88; P less than 0.05). Verbal long-term memory was also affected, but only in the simulated-ascent group; of a total of 10 words, an average of 8.14 +/- 1.86 were recalled before simulated ascent, but only 6.83 +/- 1.47 afterward (P less than 0.05). On the aphasia screening test, on which normal persons make an average of less than one error in verbal expression, the mountaineers made twice as many aphasic errors after ascent (1.03 +/- 1.10) as before (0.52 +/- 0.80; P less than 0.05). A higher ventilatory response to hypoxia correlated with a reduction in verbal learning (r = -0.88, P less than 0.05) and with poor long-term verbal memory (r = -0.99, P less than 0.01) after ascent. An increase in the number of aphasic errors on the aphasia screening test also correlated with a higher ventilatory response to hypoxia in both the simulated-ascent group (r = 0.94, P less than 0.01) and a subgroup of 11 mountaineers (r = 0.59, P less than 0.05). We conclude that persons with a more vigorous ventilatory response to hypoxia have more residual neurobehavioral impairment after returning to lower elevations. This finding may be explained by poorer oxygenation of the brain despite greater ventilation, perhaps because of a decrease in cerebral blood flow caused by hypocapnia that more than offsets the increase in arterial oxygen saturation. SO - N Engl J Med 1989 Dec 21;321(25):1714-9 AU - Regard M AU - Oelz O AU - Brugger P AU - Landis T TI - Persistent cognitive impairment in climbers after repeated exposure to extreme altitude. AB - We performed neuropsychological testing in eight world class climbers who had reached summits higher than 8,500 meters without supplementary oxygen. Five had mildly impaired concentration, short- term memory, and ability to shift concepts and control errors. There were no defects in perception or other cognitive activities. The pattern of impairment suggests malfunctioning of bifronto-temporo- limbic structures. Repeated extreme-altitude exposure can cause mild but persistent cognitive impairment. SO - Neurology 1989 Feb;39(2 Pt 1):210- From: Jeff turbo Deifik <firstname.lastname@example.org> > > Acetazolamide (AMS) > > Methylprednisolone (HACE) > > I spoke with Dr William Forgey about a year ago about HAPE. > Among other wilderness medicine books, he wrote > "Wilderness Medicine 4th Edition" > > Since I have gotten HAPE, at only 11.2k feet, the subject is important to > me. I have tried diamox and dexamethasone. They didn't help once symptoms developed. > I hiked down, starting at 1am, for about 6 miles. > > Forgey said the drug of choice is Procardia (nifediprine) 20 mg every 8 hours during > ascent, and for 3 additional days at altitude. This is relativly new information. The > book was published 3/95. I haven't had a chance to try procardia. It works by relaxing > the pulminary artery, which is what is belived to cause HAPE. Jeff turbo Deifik email@example.com firstname.lastname@example.org -- Looking for an H-912 (container).
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