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DIABETES MELLITUS TIPO 1 Y ALTITUD

Los diabéticos son uno de los colectivos mas estimulados para practicar deporte, como parte del control metabólico de su enfermedad. Se dispone de literatura médica que describe los resultados de diversas expediciones de jóvenes diabéticos tipo 1 a montañas de gran altura. La primera de estas expediciones (Kilimanjaro 2.001) no tuvo unos resultados estimulantes. El control metabólico de cada montañero se llevaba desde el equipo médico y la mayor parte se trataba profilácticamente con acetazolamida. Aunque 6 de los 15 diabéticos subieron a la cima, la expedición refirió diversos problemas: los glucómetros no fueron fiables, el control metabólico fue deficiente apareciendo diversos episodios de hipoglucemia y de cetosis,  tres casos de edema pulmonar y otro de edema cerebral de altura. Dos de los diabéticos, que seguían tratamiento profiláctico con acetazolamida, necesitaron tratamiento hospitalario por cetoacidosis grave. A posteriori, el mal resultado se atribuyó a tres errores de bulto. A) El Kilimanjaro es la montaña con mayor tasa de MAM (ver bibliografía), lo que se atribuye a una organización rígida que no permite subir al ritmo personal y por lo tanto es la montaña la menos adecuada para una expedición de este tipo. B) El mejor control glicémico se consigue cuando los diabéticos manejan su glicemia personalmente según sus circunstancias y no con un patrón rígido. C) La acetazolamida produce acidosis metabólica por lo que no es recomendable para los diabéticos sin un control muy estricto.
Posteriormente, otras expediciones de diabéticos (Aconcagua 2001, Cho Oyu 2003 y Pico Lenin 2005) fueron exitosas, con buen control de la glicemia y sin presentar mayores complicaciones que dos casos de deshidratación con disminución de la conciencia y de la capacidad de controles metabólicos seguida de descompensación diabética. Estos dos casos de deshidratación son un número similar al que aparece en expediciones de montañeros no diabéticos. Naturalmente que en un diabético es mas grave porque pierde la capacidad de controlar su glicemia.

Los conocimientos actuales se resumen en:
1. En teoría la adrenergia y el aumento de la secreción de cortisol debieran aumentar la glicemia o la necesidad de insulina, pero los estudios practicados en cámara hipobárica no han mostrado efecto de la hipoxia por si sola en el control de la diabetes.
2. Las evaluaciones sobre el terreno, si que muestran cierta tendencia al aumento de la glicemia o de las necesidades de insulina durante las ascensiones. Se atribuye al estrés, a la mayor secreción de hormonas contrarreguladoras o a la disminución del ejercicio real que se produce en la altura. La mayor parte de los alpinistas o atletas diabéticos, que siguen buen control de su glicemia a nivel del mar no tienen mayores dificultades para continuar haciéndolo en la altura. 
3. Las dificultades técnicas tienen importancia. Son necesarios ciertos conocimientos e infraestructura como llevar el glucómetro, la insulina y el resto del equipo junto al cuerpo para evitar su congelación, saberlo manejar sin desprenderse de las manoplas o a través de la ropa, disponer de los alimentos adecuados, etc. Existen unas recomendaciones de la International Society of Mountain Medicine (ISMM) sobre este apartado.
4. Los viajes transoceánicos, que alargan o acortan el día, comportan irregularidad en el horario de la ingesta y de la administración de insulina, lo que efecta al control de la diabetes.
5. El MAM no es mas frecuente entre los diabéticos que en el resto de los viajeros. En los diabéticos se contraindican formalmente los fármacos considerados profilácticos del mal de montaña (dexametasona y acetazolamida).
En resumen: los diabéticos capaces de controlarse bien y sin complicaciones, pueden ascender, hacer ejercicio y mostrar las mismas capacidades que los demás. Pero si hay problemas (accidente, disminución de la capacidad de autorregulación, quedarse sin comida o sin insulina por pérdida del equipo, deshidratación por diarreas, etc. que son situaciones comunes en la montaña) su capacidad de supervivencia está muy disminuida. El papel de los compañeros es básico, debiendo poder reconocer una hipoglicemia y disponiendo en todo momento de recambio del equipo mínimo y de emergencia.

RECOMENDACIONES DE LA ISMM.

Respecto del alpinista.
1. Escoger bien los objetivos según las capacidades.
2. Tratamiento flexible según la situación.
3. Controles frecuentes bajo cualquier circunstancia especialmente antes de las situaciones expuestas y después de las comidas.
4. Capacidad de calcular los carbohidratos, el ejercicio y la necesidad de insulina.
5. Ser consciente de que estas habilidades se pueden ver afectadas en la altura.
6. Habilidad para reconocer y tratar la hipoglicemia y la hiperglicemia.
7. Examen de la retina antes de las ascensiones a gran altura.

Respecto del equipo y de la insulina.
1. Recambios abundantes de todo el equipo necesario en diferentes mochilas, bidones, etc (insulina, glucagon, carbohidratos de emergencia, glucómetros, etc).
2. Métodos alternativos para medir la glucosa (tiras reactivas, diferentes glucómetros) o para administrar insulina (bomba continua, diferentes jeringas).
3. Bolsillos aislantes situados cercanos al cuerpo para los glucómetros y la insulina.
4. Acceso fàcil a todo el equipo, especialmente al glucagon y a la insulina.
5. Volver a bajar el equipo desechable usado. No dejar nada en la montaña.

Respecto de los miembros del grupo.
1. Conocer como actuar en caso de emergencias como la hipoglicemia o la cetoacidosis.
2. Conocer el equipo y donde se almacena o se transporta.
Respecto de la aclimatación.
1. Aclimatación lenta para evitar el Mal de Montaña.
2. Se contraindican los medicamentos “preventivos” (acetazolamida, dexametasona).
3. Ser consciente de que el edema pulmonar i cerebral de altura puede complicar una descompensación diabética y viceversa.


BIBLIOGRAFÍA DIABETES Y ALTURA.
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2. Adiq. Alpinisti diabetici in alta quota. www.adiq.org 
3. Admetlla J., Leal C., and Ricart A. (2001). Management of diabetes at high altitude. Br. J. Sports Med. 35:282.
4. Admetlla J., Leal C., and Ricart A. (2003). Diabetes mellitus and mountain sports in health & height. Proceedings of the 5th World Congress on Mountain Medicine and High Altitude Physiology. G. Viscor, A. Ricart, and C. Leal, eds. Publicacions de la Universitat de Barcelona, Barcelona, Spain; pp. 229–236.
5. Barreau P.B., and Buttery J.E. (1988). Effect of hematocrit concentration on blood glucose value determined on Glucometer II. Diabetes Care 11(2):116–118.
6. Basnyat B. (1995). Himalaya Rescue Association. Diabetic ketoacidosis in mountain trekkers. ISMM Newsletter 5(3):4–5.
7. Bladé E. (1996). Expedició UPC-Everest 95. Esport i Vida. 13 AIED; pp. 12–13.
8. Brooks G.A., Butterfield G.E., Wolfe R.R., Groves B.M., Mazzeo R.S., Sutton J.R., Wolfel E.E., and Reeves J.T. (1991). Increased dependence on blood glucose after acclimatization to 4,300 m. J. Appl. Physiol. 70:919–927.
9. Chandran M., and Edelman, S. (2003). Have insulin, will fly: Diabetes management during air travel and time zone adjustment strategies. Clin. Diabetes 21(2):82–84.
10. Chartier P. (1992). Oedème cérébral de haute altitude au Hinku (Nepal). Bulletin de l’Arpe; pp. 3–4.
11. Currie C.J., Lacey L., and Peters J.R. (1999). Changes in glucose tolerance at high altitude. Diabetes 48 (Suppl):A399–400.
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13. Favier Roland J.M. (2000). The effects of altitude on the hormonal responses to exercise. In: Sports Endocrinology. M.P. Warren, ed. Humana Press, Totowa, NJ; pp. 371–389.
14. Fleming D.R., Jacober S.J., Vandenberg M.A., Fitzgerald J., and Grunberger G. (1997). The safety of injecting insulin through clothing. Diabetes Care 20(3):244–247.
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17. Giné R. (1997b). La conquesta de l’Everest. Esport i Vida 16 AIED; pp. 26–30.
18. Giordano, B.P., Thrash W., Hollenbaugh L., Dube W.P., Hodges C., Swain A., Banion C.R., and Klingensmith G.J. (1989). Performance of seven blood glucose testing systems at high altitude. Diabetes Education 15(5):444–448.
19. Hackett P.H. (2001). High altitude and common medical conditions. In: High Altitude. An Exploration of Human Adaptation. Ed. T.F. Hornbein and R. B. Schoene, eds. Marcel Dekker, New York–Basel; p. 866.
20. Heath D., and Williams D. (1981). Man at High Altitude 2nd ed; pp. 254–255.
21. Herter C.D. (1999). DKA on Mont Rainier: A case report. Diabetes Spectrum 12(4):198–200. 
22. Larsen J.J., Hansen J.M., Olsen N.V., Galbo H., and Dela F. (1997). The effect of altitude on glucose homeostasis in men. J. Physiol. 504(1):241–249.
23. Leal C. (2000) Diabetes en la montaña. El Passamuntanyes 17:12–15.
24. Leal C. (2005) Goig High with Type 1 Diabetes. High Altitude Medicina & Biology. 6(1):14-21.
25. Martínez F. (1990). Glicemia y altura extrema. In: Adaptación Humana a la Altura. Expedición Médica Cho Oyu. Instituto Municipal del Deporte Vitoria Gasteiz España, pp. 129–130.
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29. Panofsky D. (2003). Handling type 1 diabetes in the mountains: Considerations for the diabetic climber in health & height. Proceedings of the 5th World Congress on Mountain Medicine and High Altitude Physiology. G. Viscor, A. Ricart, and C. Leal, eds. Publicacions de la Universitat de Barcelona, Barcelona, Spain; pp. 237–241.
30. Pavan P., Sarto P., Merlo L., Casar D., Ponchia A., Biasin R., Noventa D., and Avogaro A. (2003). Extreme altitude mountaineering and type 1 diabetes. The Cho Oyu alpinisti in alta quota expedition. Diabetes Care 26(1):3196–3197.
31. Pavan P., Sarto P., Merlo L., Casar D., Ponchia A., Biasin R., Noventa D., and Avogaro A. (2004). Metabolic and cardiovascular parameters in type 1 diabetes at extreme altitude. Med. Sci. Sports Exerc. 36(8):1283–1289.
32. Pecchio O., Maule S., Migliardi M., Trento M., and Veglio M. (2000). Effects of exposure at an altitude of 3000m on performance of glucometers. Diabetes Care 23(1):129–131.
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35. Richalet J.P. (2001). The endocrine system. In: High Altitude. An Exploration of Human Adaptation. T.F. Hornbein and R.B. Schoene, eds. Marcel Dekker, New York–Basel; pp. 623–624.
36. Sawhney R.C., Malhotra A.S., and Singh T. (1991). Glucoregulatory hormones in man at high altitude. Eur. J. Appl. Physiol. Occup. Physiol. 62:286–291.
37. Shlim D.R., and Gallie J. (1992). The causes of death among trekkers in Nepal. Int. J. Sports Med. 13:74–76.
38. Sutton J.R., Viol G.W., Gray G.W., McFadden M.D., and Keane P.M. (1977). Renin, aldosterone, electrolyte and cortisol responses to hypoxic decompression. J. Appl. Physiol. 43:421–424.
39. Swenson E. (2000). Respiratory and renal roles of carbonic anhydrase in gas exchange and acid–base regulation. In: The Carbonic Anhydrases. New Horizons. W.R. Chegwidden, N.D. Carter, and Y.H. Edwards, eds. Birkhäuser Verlag, Basel, Switzerland; pp. 313–314.
40. Ward M., Milledge J., and West J. (2000). Exercise. In: High Altitude Medicine and Physiology, 3rd ed. Oxford University Press, New York; p. 139.
41. Williams R.A., and Petoskey M. (2000). Blood glucose monitoring at high altitude (letter). Diabetes Spectrum 13(2):79.

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ACUTE HYPOBARIC HIPOXIA DOES NOT AFFECT THE INSULIN REQUIREMENT IN WELL-CONTROLLED DIABETICS.
Conxita Leal, Jordi Admetlla,Teresa Pagés, Ginés Viscor, Antoni Ricart 

Introduction
The effects of acute hypoxia on the metabolism of glycemia in patients with type 1 diabetes mellitus are little known. The data we have at present are based on the study of diabetic alpinists at high altitude. Exposure to altitude implies an increase of the activity of counterinsulin hormones, which has led to the supposition that at high altitudes higher doses of insulin would be required. However, previous field studies (Admetlla 2002) are not conclusive. 

Materials and methods
To clarify the role of acute hypoxia in the metabolism of glucose and in the sensitivity to insulin, 6 diabetic subjects, 5 of whom had wide previous experience at high altitude, were submitted to 2 sessions of 3 hours’ duration each in a hypobaric chamber, during which the subjects’ glycemia was monitored by continuous recording sensors. The work protocol was approved (20 April 2005) by the Bioethics Committee of the Universidad de Barcelona (Institutional Review Board IRB00003099). All the subjects were given a complete medical check-up at the beginning of the study and agreed to follow the general guidelines in their diet and physical activity for the whole duration of the study.

The study lasted for four days, during which the physical activity and the diet of the participants was monitored. Each subject self-managed and self-reported both the physical activity and the diet, which were similar each day.  On the first day, the glucose sensors were implanted and the subjects were allowed to familiarize themselves with the operation of these devices. On the two complete recording days that followed, a morning schedule (9:00-13:00h) was developed of sessions in the hypobaric chamber, although only on the second occasion was the vacuum system used, attaining a simulated altitude condition equivalent to 5000m. In this way, it was possible to compare the values and tendencies in all the parameters between both days (controls in normoxia and in hypoxia). On the fourth day, only the collection of morning urine samples were carried out and the data of the monitoring teams were recovered.

On the morning of the first day of the study, the subjects were implanted with a subcutaneous glucose sensor (CGMSgold Medtronic Mini-Med, Sylmar, CA, USA). This device continued to function until the morning of the fourth day. Following the manufacturer’s instructions, each subject calibrated their own instrument at least 4 times each day with the glycemia values obtained in a capillary sample from the middle finger of the hand. On the second and third days, two blood extractions were drawn from an antecubital vein for all the subjects participating in the study: one prior to beginning and the other on ending the morning session in the hypobaric chamber. The parameters analyzed were: the red series, glucose, glucagon, cortisol, growth hormone, insulin, C-peptide, and vanillylmandelic acid (VMA). Cortisol was determined via a urine sample collected from the first morning urine. All the analyses were carried out by a homologated laboratory by standard means. Physical activity was monitored by a podometer, along with the diet and insulin dosage via various questionnaires, in each one of the subjects on the days of data collection. 

Results and conclusions
The diet, the exercise, and the glycemia variations throughout the day were similar on both days, the one for normoxia and the one for hypoxia. No significant differences were found in any of the parameters measured between normoxia and hypoxia. These findings appear to indicate that hypoxia itself does not have a determining effect on glycemia in well-controlled diabetics, which is not surprising if we consider that for obvious reasons of ethics and security the administration of insulin in the patients was not restricted. However, there was no variation in the insulin requirements between the two days, either, which shows that neither sensitivity to insulin nor the net rate of glucose use is affected by an acute hypobaric hypoxia.

It must be noted that the study has an important limitation imposed by the design itself: the exposure to hypoxia was acute—intense and short. For this reason, the results cannot be extrapolated to other real situations on the mountain, where diet and exercise are not controlled, or where other factors can influence, such as the degree of individual acclimatation, the cold, or fatigue. Studies will be needed with more prolonged or intermittent exposures to define the response of diabetics to altitude.
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Dolor Neurític en Expedicions

NEUROPATHIC PAIN AFTER HIMALAYAN EXPEDITIONS.

Antoni Ricart de Mesones, MD; Janina Turón Sans, MD;  Mercedes Misiego, MD; Hisao Onaga Pueyo, MD; Rosa Real Soriano, MD; and Javier Botella de Maglia, MD.

From the Mountain Medicine Studies Institute Dr. Castelló Roca (IEMM), (Drs. A. Ricart de Mesones, H. Onaga Pueyo, and J. Botella de Maglia), the Spanish Society for Mountain Medicine (Drs. A. Ricart de Mesones, R. Real Soriano, and J. Botella de Maglia); and the Department of Neurology, Bellvitge University Hospital, Barcelona (Dr. J. Turón Sans).

Abstract 
High-altitude peripheral nerve disease secondary to frostbite or trauma is a well-recognized medical problem during mountaineering expeditions. However, in our experience of medical professionals on 19 expeditions to the Himalayas in the years 1977–2000, an unusual syndrome of neuropathic pain and/or dysesthesia in both feet apparently unrelated to frostbite or trench foot was observed in 8 (4.8%) of 165 European mountaineers. Mountaineers complained of persistent and continuous pain, which was consistently described as a ‘corky feeling’ sensation in their feet, associated with severe lancinating exacerbations. Pain improved with cold and worsened with heat and gentle pressure. Symptoms were incapacitating in a third of cases. Treatment with carbamazepine was effective and the disorder evolved to total resolution in 4–8 weeks. We present the case of a patient who had this syndrome and in whom complete work-up studies done on his arrival home, 14 days after its presentation, were unrevealing. The paucity of information regarding this particular variety of neuropathic pain of the feet may be due to lack of clinical suspicion in the field, favorable outcome, and difficulties for further study and evaluation.

Introduction
Some physicians with large experience in high-altitude expeditions are familiar with a clinical condition characterized by unexplained pain and dysesthesia in both feet during expeditions to Himalaya or Karakoram. Although this particular variety of neuropathic pain without any visible injury of the tissues, apparently unrelated to frostbite, known trauma or trench foot, has previously been reported in non-English language journals (Villas et al, 1982, 1984; Ricart de Mesones, 1994, 2000; Turón et al, 2000; Real et al, 2001), language barriers prevented accessibility of the incidence, clinical features, and prognosis of this medical illness to the international literature. This case report of a patient who has recently been studied and followed up by our group illustrates several characteristics of neuropathic pain of the feet in European mountaineers.

Case:
A group of three mountaineers opened a new route in the North Face of Amin Brakk (5,850 m) in Karakoram. The climb was extremely difficult (A5/6ºc+/60º), long (1,650 m), humid, and moderately cold. A duration of 27 days was foreseen but the climb took 5 days more; therefore, water and food were rationed. The mean temperature was 0ºC and the equipment was the appropriate for a climb of these characteristics. When returned to the base camp at 4,600 m, a 37-year-old man suffered from pain and dysesthesia in the soles and toes, slightly more severe on the left foot. Pain was intense and continuous with acute burning exacerbations accompanied by bradycardia and diaphoresis. It improved with cold and worsened with warmth inside the sleeping bag. Painful areas showed a sock-like distribution in both feet with distal predominance. There was a decrease of epicritic sensitivity, which was described by the patient as ‘corky toes’. Pain was elicited by minor contacts, e.g. the smooth contact of bedclothes. The patient feared to have suffered from frostbite but he could not remember when or how could he have had their feet frostbitten. Five days later, he consulted with two of the authors who at this time were taking part in another expedition (Real et al, 2001). The patient was treated with carbamazepine, 200 mg every 8 hours, and marked relief of pain was obtained. On his arrival home, 14 days after his initial presentation, he was studied in our hospital.
On admission the patient had dysesthesia and pain in both feet. The pain intensity was 2 in a scale from 0 to 10 (it had been 8 at the beginning of the illness). The map of the sensitive dysfunction is shown in Figures 1 and 2. No motor deficits or impairment of patellar or Achilles tendon reflexes were observed. The skin temperature, color, and morphological appearance of the lower extremities were normal (the consultation room temperature was 22ºC). There were no visible lesions suggesting frostbite, inflammation or ischemia. Physical examination of pulses and circulation of the extremities were normal. Neither passive nor active movements of the joints produced pain but blunt or rubbing contact to the skin evoked a painful feeling. When the patient’s feet were exposed to cold, toes became cyanotic suggesting intense vasoconstriction and the patient referred pain improvement. By contrast, hyperemia and pain were related to warmth. Conventional sensitive electroneurography was normal, as well as the quantitative thermotest (analysis of thresholds for cold, heat, and pain induced by cold and heat). Laboratory tests were unrevealing except for hepatic dysfunction, which was attributed to treatment with carbamazepine, and a subclinical hypothyroidism. However, thyroid function tests returned to normal values without treatment and liver function tests normalized after withdrawal of carbamazepine treatment. Invasive studies such as neural and muscle biopsies were not indicated because of the favorable patient’s clinical course with complete disappearance of signs and symptoms after 5 weeks.

Epidemiological data
In our experience of medical professionals on 19 expeditions to the Himalayas in the years 1977–2000, a syndrome of neuropathic pain and dysesthesia in both feet, without any clinical sign of tissue injury due to cold, “immersion or trench foot” or trauma was observed in 8 (4.8%) of 165 European mountaineers (Table 1). Some of the 165 mountaineers suffered from frostbite or different kinds of tissue injuries. Neuropathic troubles related to any kind of visible tissue injury, frostbite or trench foot were excluded of the table.
No Hunza, Balti, Sherpa or Tibetan high-altitude porters consulted during the expedition for pain or dysesthesia related to this syndrome. 
In all cases, the pain or dysesthesia appeared during descent to the base camp after a stay longer than two weeks climbing at altitudes above 6,000 m except in the case of the Amin Brakk and Manaslu. In all cases, mountaineers were well acclimatized and in good physical condition. In five cases the climbers were coming back from an eight thousand meters summit, or attempt to summit. Two cases appeared in mountaineers after some fruitless days waiting in a high camp due to bad weather; so, soft socks were used inside the tents much longer than hard boots or crampons. 
Motor deficit, propioceptive disturbances or dificulties for walking (except severe pain) were never seen. 
The disorder disappeared progressively over 4–8 weeks, seemingly without sequelae. Most affected mountaineers have not suffered from relapses even in later expeditions and similar conditions. In one case, pain lasted several months and became more intense when the subject came back from several hours of mountain activities, with no relation to cold. Neuralgia was severe and incapacitating only in three cases. The remaining five mountaineers could walk along the descent march. Analgesic treatment brought about a transient improvement of pain. Treatment with acetylsalicylic acid, non-steroidal antiinflamatory drugs or vitamin B did not improve the pain. In all cases pain disappeared before resolution of dysesthesia. Two subjects treated with carbamazepine showed clear improvement of symptoms, but the effect of this drug on the time-course of the disease is unknown.

Table. Occurrence of neuropathic pain among 165 European mountaineers.
The table includes only the neuropathic nuisances with normal skin (except vasoconstriction with cold and hyperemia with warmth). Neuropathic troubles related to frostbite, trench foot or trauma were excluded of the table.


Figures 1 and 2: Limits of dysesthesia for sense of touch (black) and thermal (cold) sense (white).


Discussion
In the early 80s, a series was reported of 12 mountaineers who consistently suffered from a loss of sensitivity in their toes without cutaneous signs of frostbite. All patients had taken part in long (11–63 hour) snow-and-ice climbs at high (but not extreme) altitudes (2,500–4,808 m). All cases presented with a ‘corky’ sensation and a reduction of the tactile and thermoalgesic sensitivity, which was not accompanied by skin paleness, cyanosis, blisters or pain. This disorder resolved spontaneously in 1–3 months without sequelae. The authors attributed this syndrome to the combined effect of cold, compression by the crampon straps and repeated microtrauma during snow-and-ice climbing, which could alter the toe irrigation and cause ischemic damage of digital collateral nerves. They proposed the term of ‘resolutive temporal hypoesthesia’ (Villas et al, 1981, 1982, 1984; Jimeno et al, 1981).
The syndrome here reported has some clinical similarities but the causative circumstances seem to be different.
At the present time, the pathogenetic mechanism of the syndrome is unknown. The lack of any visible injury makes hard to support the diagnosis of frostbite, trench foot or trauma. The clinical features of the pain point toward the neuropathic origin of the disorder, which is further supported by the patients clinical improvement with carbamazepine, a drug which blocks sodium channels. The fact that the syndrome is only seen in the lower extremities points out to some factor related to the longer axons. The pressure neuropathy, as suggested in the first paragraph, can not be excluded as a trigger or worsening factor, but the different circumstances of the presentation and the lack of motor or propioceptive affectation points out to small fiber polyneuropathy.
This small fiber polyneuropathy reminds the ABC syndrome (Angry Backfiring C-nociceptor), erythromelalgia or erythralgia, characterized by a warm, red limb which is hyperalgesic to heat (Cline et al, 1989; Culp et al, 1989; Campero et al, 1996; Layzer, 2001). Microvascular arteriovenous shunting and/or changes in the threshold for pain of the unmyelinated C polymodal nociceptors have been shown to play a role in the pathogenetic mechanism of this condition (Yarnitsky, 1990; Mork, 2000). On the other hand, the syndrome has been associated to different disorders including among others diabetes mellitus, metabolic or nutritional deficiencies, hematologic diseases, amyloidosis, intoxications, AIDS, and infection. All the common causes of this type of polyneuropathies must be considered, but most of these factors can be easily excluded in young healthy mountaineers. It should be noted that the majority of small caliber nerve fiber polyneuropathies are of unknown cause.
The etiology of this disorder should probably be sought among metabolic or nutritional problems, cold or altitude effects, perhaps worsened by hemoconcentration, local pressure or other factors. If nutrition, altitude or pressure were the unique etiology of the dysfunction, it would be expected for the symptoms to appear during the stay at high altitude. But in all cases symptoms appeared during or few hours after the descent. This fact suggests that some factors, maybe cold, might mask the appearance of symptoms at high altitude, since patients referred pain relief in contact with cold. The syndrome classification of these patients is essential in order to define the pathophysiology and to lead to a correct prevention and treatment. But, if the etiology is unknown and the cause no longer acts, the treatment can only be symptomatic. In the case here reported, the main symptom was neuropathic pain that responded to treatment with carbamazepine. Diagnosis on the field is based on clinical features, but specific diagnostic techniques for assessing small caliber nerve fiber neuropathy are required to confirm the diagnosis because, in these patients, results of standard tests are usually unrevealing.


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