Mal de montaña de tipo agudo, subagudo y crónico / Acute, subacute and chronic mountain sickness

Más de 100 millones de personas ascienden cada año a áreas montañosas elevadas en todo el planeta y en altitudes no extremas (< 5.500 m) entre el 10 y el 85% se ven afectados por el denominado mal agudo de montaña, la enfermedad más frecuentemente inducida por una hipoxia hipobárica ligera-moderada. Asimismo, unos 140 millones de seres humanos viven de forma permanente en cotas comprendidas entre 2.500-5.500 m y hasta un 10% de ellos padecen la forma subaguda del mal de montaña (hipertensión pulmonar de la gran altitud) o la forma crónica (enfermedad de Monge), esta última especialmente frecuente en etnias andinas. La presente revisión expone los conceptos generales más relevantes en torno a estas 3variantes clínicas, las cuales pueden ser incapacitantes, llegar a complicarse y ser potencialmente mortales, siendo esencial realizar una correcta prevención, diagnóstico, terapéutica y manejo de las mismas en un entorno hostil como es la alta montaña (AU)

More than 100 million people ascend to high mountainous areas worldwide every year. At nonextreme altitudes (<5500 m), 10–85% of these individuals are affected by acute mountain sickness, the most common disease induced by mild-moderate hypobaric hypoxia. Approximately 140 million individuals live permanently at heights of 2500–5500 m, and up to 10% of them are affected by the subacute form of mountain sickness (high-altitude pulmonary hypertension) or the chronic form (Monge's disease), the latter of which is especially common in Andean ethnicities. This review presents the most relevant general concepts of these 3 clinical variants, which can be incapacitating and can result in complications and become life-threatening. Proper prevention, diagnosis, treatment and management of these conditions in a hostile environment such as high mountains are therefore essential (AU)

Acute, subacute and chronic mountain sickness.

More than 100 million people ascend to high mountainous areas worldwide every year. At nonextreme altitudes (<5500m), 10-85% of these individuals are affected by acute mountain sickness, the most common disease induced by mild-moderate hypobaric hypoxia. Approximately 140 million individuals live permanently at heights of 2500-5500m, and up to 10% of them are affected by the subacute form of mountain sickness (high-altitude pulmonary hypertension) or the chronic form (Monge's disease), the latter of which is especially common in Andean ethnicities. This review presents the most relevant general concepts of these 3 clinical variants, which can be incapacitating and can result in complications and become life-threatening. Proper prevention, diagnosis, treatment and management of these conditions in a hostile environment such as high mountains are therefore essential.

Acute, subacute and chronic mountain sickness. / Mal de montaña de tipo agudo, subagudo y crónico.

More than 100 million people ascend to high mountainous areas worldwide every year. At nonextreme altitudes (<5500 m), 10-85% of these individuals are affected by acute mountain sickness, the most common disease induced by mild-moderate hypobaric hypoxia. Approximately 140 million individuals live permanently at heights of 2500-5500 m, and up to 10% of them are affected by the subacute form of mountain sickness (high-altitude pulmonary hypertension) or the chronic form (Monge's disease), the latter of which is especially common in Andean ethnicities. This review presents the most relevant general concepts of these 3 clinical variants, which can be incapacitating and can result in complications and become life-threatening. Proper prevention, diagnosis, treatment and management of these conditions in a hostile environment such as high mountains are therefore essential.

[Arterial oxygen saturation during ascent of a mountain higher than 8,000 meters]. / Saturación arterial de oxígeno durante la ascensión a una montaña de más de 8.000 metros.

BACKGROUND: Arterial oxygen saturation (SaO2) diminishes with altitude. AIM: To know the values of SaO2 in healthy mountaineers during the ascent of a mountain higher than 8,000 metres. METHOD: On occasion of an expedition to Gasher brum II (8,035 m), SaO2 at rest was measured by pulse oxymetry during the approach march, in the base camp (on day one and one month later), in camps II and III, during the assault at 7,500 m and on the summit. RESULTS: During the approach march, the SaO2 in Paiju (3,365 m) was 92.9 +/- 1.4% and in Gore II (4,250 m) 85.0 +/- 4.3%. In the base camp (5,200 m) it was 78.4 +/- 9.5% on the first day and 87.4 +/- 3.0% one month later (p < 0.007). In camp II (6,500 m) it was 72.7 +/- 6.7%. In camp III (7,000 m) it was 68.0 +/- 9.3% (recorded on 21 asymptomatic climbers). At this altitude a SaO2 of 40% was recorded during sleep in an asymptomatic subject, apparently without apnoeic crises. During the assault at 7,500 m, SaO2 was 60.5 +/- 13.5% (measured on 4 climbers). On the summit (8,035 m) the SaO2 of two subjects was 84% and 88%, respectively. CONCLUSION: During expeditions to mountains higher than 8,000 metres, mountaineers have extremely low values of SaO2, similar to those of patients with severe respiratory failure. SaO2 increases progressively with acclimatization. SaO2 on the summit could have been relatively high, probably because of hyperventilation.

Saturación arterial de oxígeno durante la ascensión a una montaña de más de 8.000 metros / Arterial Oxygen saturation during ascent of a mountain higher than 8.000 meters

Fundamento. La saturación arterial de oxígeno (SaO2) disminuye con la altitud.Objetivo. Conocer qué SaO2 presentan los montañeros sanos durante la ascensión a una montaña de más de 8.000 metros.Método. En una expedición al Gasherbrum II (8.035 m) se midió la SaO2 por pulsioximetría durante la marcha de aproximación, en el campamento base (a la llegada y un mes después), en los campamentos II y III, a 7.500 m durante el ataque y en la cumbre.Resultados. En la marcha de aproximación la SaO2 en Paiyu (3.365 m) fue del 92,9 ± 1,4% y en Gore II (4.250 m) del 85,0 ± 4,3%. En el campamento base (5.200 m) a la llegada fue del 78,4 ± 9,5% y un mes después del 87,4 ± 3,0% (p < 0,007). En el campamento II (6.500 m) fue del 72,7 ± 6,7%. En el campamento III (7.000 m) fue del 68,0 ± 9,3% (medida sobre 21 sujetos). A esta altitud se registró una SaO2 del 40% durante el sueño en unsujeto asintomático. A 7.500 m fue del 60,5 ± 13,5% (4 sujetos). En la cumbre (8.035 m) la SaO2 de dos sujetos fue del 84 y 88% respectivamente.Conclusión. Durante las expediciones a montañasde más de 8.000 m los montañeros presentan cifras de SaO2 muy bajas, comparables a las de los pacientes con insuficiencia respiratoria grave. La SaO2 aumenta progresivamente con la aclimatación. Es posible que la SaO2 en la cima del Gasherbrum II fuera relativamente alta, probablemente a consecuencia de la hiperventilación

Background. Arterial oxygen saturation (SaO2) diminishes with altitude.Aim. To know the values of SaO2 in healthy mountaineers during the ascent of a mountain higher than 8,000 metres.Method. On occasion of an expedition to Gasherbrum II (8,035 m), SaO2 at rest was measured by pulse oxymetry during the approach march, in the base camp (on day one and one month later), in camps II and III, during the assault at 7,500 m and on the summit.Results. During the approach march, the SaO2 in Paiju (3,365 m) was 92.9 ± 1.4% and in Gore II (4,250 m) 85.0 ± 4.3%. In the base camp (5,200 m) it was 78.4 ± 9.5% on the first day and 87.4 ± 3.0% one month later (p < 0.007). In camp II (6,500 m) it was 72.7 ± 6.7%. In camp III (7,000 m) it was 68.0 ± 9.3% (recorded on 21 asymptomatic climbers). At this altitude a SaO2 of 40% was recorded during sleep in an asymptomatic subject, apparently without apnoeic crises. During the assault at7,500 m, SaO2 was 60.5 ± 13.5% (measured on 4 climbers). On the summit (8,035 m) the SaO2 of two subjects was 84% and 88%, respectively.Conclusion. During expeditions to mountainshigher than 8,000 metres, mountaineers have extremely low values of SaO2, similar to those of patientswith severe respiratory failure. SaO2 increasesprogressively with acclimatization. SaO2 on the summit could have been relatively high, probably because of hyperventilation

[Changes in spirometric parameters and arterial oxygen saturation during a mountain ascent to over 3000 meters]. / Cambios espirométricos y en la saturación arterial de oxígeno durante la ascensión a una montaña de más de 3.000 metros.

OBJECTIVE: To ascertain whether climbing a mountain over 3000 meters high produces any alterations in ventilation, whether such alterations are modified by acclimatization, and whether they correlate with changes in arterial oxygen saturation (SaO2) or the development of acute mountain sickness (AMS). SUBJECTS AND METHODS: The following parameters were measured in 8 unacclimatized mountaineers who climbed Aneto (3404 m) and spent 3 days at the summit: forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), airway response to inhaled terbutaline, SaO2, and the symptoms of AMS. RESULTS: At the summit, mean (SD) FEV1 declined by 12.3% (5.7%) and mean FVC by 7.6% (6.7%) while the ratio of FEV1 to FVC remained normal. The means for both parameters were higher on the following day. No airway response to bronchodilator treatment was observed. The restriction disappeared entirely on descent. At the peak, SaO2 increased progressively as the climbers became acclimatized. During the ascent, FEV1 correlated with SaO2 (r=0.79). One participant who suffered from AMS had a ratio of FEV1 to FVC less than 70% and the worst SaO2 during the 3 days on the summit. Obstruction preceded the AMS symptoms, did not respond to bronchodilator treatment, and disappeared when the climber descended. CONCLUSIONS: The mountaineers who climbed over 3000 meters presented restriction that correlated with hypoxemia. This restriction did not respond to bronchodilator treatment, improved with acclimatization, and disappeared on descent. One person with AMS presented obstruction that did not respond to terbutaline and disappeared on descent.

Cambios espirométricos y en la saturación arterial de oxígeno durante la ascensión a una montaña de más de 3.000 metros / Changes in spirometric parameters and arterial oxygen saturation during a mountain ascent to over 3000 meters

Objetivo: Averiguar si en la ascensión a una montaña de más de 3.000 m se produce alguna alteración ventilatoria, si ésta se modifica por la aclimatación y si se relaciona con los cambios en la saturación arterial de oxígeno (SaO2) o con la aparición de síntomas de mal de montaña agudo (MAM). Sujetos y métodos: En 8 montañeros no aclimatados que ascendieron a la cumbre del Aneto (3.404 m) y permanecieron 3 días en ella medimos: la capacidad vital forzada (FVC), el volumen espiratorio forzado en el primer segundo (FEV1), la respuesta a la inhalación de terbutalina, la SaO2 y los síntomas de MAM. Resultados: Al llegar a la cumbre disminuyeron el FEV1 (12,3 ± 5,7%) y la FVC (7,6 ± 6,7%) con la relación FEV1/FVC% normal. Al día siguiente aumentaron ambos parámetros. No hubo respuesta al tratamiento broncodilatador. La restricción se corrigió totalmente al descender. La SaO2 en la cumbre aumentó progresivamente con la aclimatación. Durante la ascensión el FEV1 se correlacionó con la SaO2 (r = 0,79). Un participante con MAM presentó FEV1/FVC menor del 70% y la peor SaO2 durante la estancia en la cima. Esta obstrucción precedió a los síntomas, no cedió con tratamiento broncodilatador y se corrigió con el descenso. Conclusiones: Los montañeros que ascienden a montañas de más de 3.000 m presentan una restricción que se correlaciona con la hipoxemia, no mejora con el tratamiento broncodilatador, se alivia con la aclimatación y desaparece con el descenso. Un sujeto con MAM sufrió una obstrucción que no respondió a la terbutalina y desapareció con el descenso

Objective: To ascertain whether climbing a mountain over 3000 meters high produces any alterations in ventilation, whether such alterations are modified by acclimatization, and whether they correlate with changes in arterial oxygen saturation (SaO2) or the development of acute mountain sickness (AMS). Subjects and methods: The following parameters were measured in 8 unacclimatized mountaineers who climbed Aneto (3404 m) and spent 3 days at the summit: forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), airway response to inhaled terbutaline, SaO2, and the symptoms of AMS. Results: At the summit, mean (SD) FEV1 declined by 12.3% (5.7%) and mean FVC by 7.6% (6.7%) while the ratio of FEV1 to FVC remained normal. The means for both parameters were higher on the following day. No airway response to bronchodilator treatment was observed. The restriction disappeared entirely on descent. At the peak, SaO2 increased progressively as the climbers became acclimatized. During the ascent, FEV1 correlated with SaO2 (r=0.79). One participant who suffered from AMS had a ratio of FEV1 to FVC less than 70% and the worst SaO2 during the 3 days on the summit. Obstruction preceded the AMS symptoms, did not respond to bronchodilator treatment, and disappeared when the climber descended. Conclusions: The mountaineers who climbed over 3000 meters presented restriction that correlated with hypoxemia. This restriction did not respond to bronchodilator treatment, improved with acclimatization, and disappeared on descent. One person with AMS presented obstruction that did not respond to terbutaline and disappeared on descent

[Triiodothyronine intoxication. A clinical and phamacokinetic study]. / Intoxicación por triyodotironina. Estudio clínico y farmacocinético.

A woman, thyroidectomised because of a thyroid papillary carcinoma, interrupted temporarily her levothyroxine intake in order to be subjected to an extension study five weeks later. To minimise her symptoms for the first three weeks, a treatment was prescribed consisting of one 25 micro g-capsule of triiodothyronine every 8 hours. Nine days later she complained of abdominal pain, nausea, vomiting, fever of 40 degrees C and chest discomfort. A serum total triiodothyronine of 575.2 nmol/l was measured by chemoluminiscent immunoassay eleven hours after the intake of the latest capsule (normal level: 1.1-2.9 nmol/l). Along the following ten days the patient suffered from delirium, agitation, tachycardia, hypertension, constipation and later diarrhoea, but neither arrythmias nor axillary temperature over 38 degrees C. Fifty-nine measurements of the serum total triiodothyronine were performed in order to determine the kinetics of elimination of this drug. We estimate that the maximal serum concentration after the intake of the latest capsule could be 794.3 nmol/l, i.e. 397 times higher than the mean normal value. The elimination half-life was 24 hours 40 minutes. The charcoal haemoperfusion had no impact on the velocity of elimination. The concentration of triiodothyronine became normal 200 hours after the intake of the latest capsule, but the clinical manifestations still lasted three days more. The pharmacokinetic data suggest that this intoxication could be due to the intake of capsules containing 5 mg of triiodothyronine, i.e. a dose 200 times higher than that prescribed by her physician.

Intoxicación por triyodotironina. Estudio clínico y farmacocinético / Triiodothyronine intoxication. A clinical and pharmacokinetic study

A una mujer tiroidectomizada por carcinoma papilar de tiroides se le suspendió el tratamiento con L-tiroxina para realizar un estudio de extensión cinco semanas después. Para minimizar sus síntomas durante las tres primeras semanas se le prescribió tratamiento con cápsulas de 25 µg de triyodotironina cada 8 horas. Nueve días después consultó por dolor abdominal, náuseas, vómitos, fiebre de 40 ºC, mareo y molestia torácica. Mediante inmunoanálisis quimioluminiscente se detectó una triyodotironina sérica total de 575,2 nmol/l a las 11 horas de la toma de la última cápsula (valor normal: 1,1-2,9 nmol/l). A lo largo de los diez días siguientes la enferma presentó delirio, agitación, taquicardia, hipertensión arterial, estreñimiento y luego diarrea, pero no arritmias ni temperatura superior a 38 ºC. Se realizaron 59 determinaciones de triyodotironina total para determinar la cinética de eliminación de esta hormona. Se calcula que la máxima concentración sérica tras la ingestión de la última cápsula debió ser de 794,3 nmol/l, es decir, 397 veces superior al promedio de la normalidad. La vida media de eliminación fue de 24 horas y 40 minutos. La hemoperfusión con carbón activado no tuvo impacto alguno sobre la velocidad de eliminación. La concentración de triyodotironina se normalizó a las 200 horas de la toma de la última cápsula, pero las manifestaciones clínicas tardaron tres días más en desaparecer. Los datos farmacocinéticos sugieren que la intoxicación pudo deberse a que durante nueve días la paciente tomara cápsulas con 5 mg de triyodotironina, es decir, una dosis 200 veces mayor que la prescrita por su médico (AU)

Los artículos de revisión deberían tener más en cuenta las publicaciones españolas / The review articles should take into account the Spanish publications

No disponible

[Paraquat poisoning. A study of 29 cases and evaluation of the effectiveness of the "Caribbean scheme"]. / Intoxicación por paraquat. Estudio de 29 casos y evaluación del tratamiento con la "pauta caribeña".

BACKGROUND: To study clinical aspects of the oral paraquat intoxication and to assess the effectiveness of both the charcoal haemoperfusion and the so-called "Caribbean scheme" (cyclophosphamide, dexamethasone, furosemide and vitamins B and C) to reduce its mortality. PATIENTS AND METHOD: Retrospective study of 29 consecutive cases admitted to our intensive care unit in 17 years. RESULTS: a) Twenty five men and four women ingested 20% paraquat solution, either accidentally (4 subjects) or deliberately (25 subjects). The suicidal purpose was particularly strong among men aged 50-66 years. Most of patients had vomits and diarrhoea. All patients developed oral and pharyngeal caustic lesions. Hypokalaemia was detected on admission in 9 patients. Increased levels of serum aminotransferases, bilirubin, amylase or creatinkinase were detected in some patients. Twenty two patients developed acute renal failure and 18 patients respiratory failure. Twenty patients died (ten in the first 48 hours and ten between days 3 and 30); b) charcoal haemoperfusion was performed on 16 patients; 4 of the 16 treated patients survived, versus 5 of the 13 non treated (p = NS), and c) the "Caribbean scheme" was applied on 18 patients. All but one of the 11 subjects who ingested >= 45 ml (treated with the "Caribbean scheme" or not) died. Among those who ingested 45 ml, 8 of the 12 treated patients survived, versus none of the 6 non treated ones (p < 0.05). CONCLUSIONS: Charcoal haemoperfusion did not reduce mortality of paraquat. The "Caribbean scheme" was associated with a lesser mortality in the subjects who ingested 45 ml of 20% paraquat solution.

[Severe and complicated malaria. Report of six cases]. / Malaria grave y complicada. Estudio de seis casos.

Six patients with severe and complicated falciparum malaria (6.7 +/- 2.7 WHO criteria) were admitted to our Intensive Care Unit. All patients acquired the disease while travelling in tropical Africa without appropriate chemoprophylaxis. The clinical manifestations included hyperpyrexia (all patients), chills (4), sweating (2), asthenia (3), anorexia (2), headache (1), arthralgias (1), vomiting (4), diarrhoea or abdominal discomfort (3), jaundice (2) and disturbances of consciousness (4). All patients had anemia, thrombocytopenia, hyponatremia, hypoproteinemia, hypoalbuminemia, hypocalcemia and acute renal failure, in one case associated with anuria. A low grade parasitemia was observed in two patients and a high grade parasitemia (20%-58% of erythrocytes) in four. Exchange transfusion was performed only in high parasitemic patients and all of them survived. All patients were treated with quinine, a sulfonamide and pyrimethamine. Additionally, five patients received oxytetracycline, doxycycline or clindamycin. Three patients required hemodyalisis. Five patients had delirium, coma or seizures. All patients had at least one sign of hepatic impairment: liver enlargement, jaundice or increased bilirubin or aminotransferase levels. Two patients had spleen enlargement. Laboratory findings suggested disseminated intravascular coagulation in four patients. Four patients developed pulmonary changes and three of them required mechanical ventilation. A Swan-Ganz catheter was placed in four patients. In three of them (two with pulmonary edema) the pulmonary capillary wedge pressure was initially increased, which suggested a cardiogenic or hypervolemia mechanism, but soon returned to normal level. One patient with low grade parasitemia died because of adult respiratory distress syndrome after 18 days. In our series, the degree of parasitemia was not related to the severity of the disease.

[Prospective study of nosocomial infections in a medical ICU. A proposal for the generalized use of the National Nosocomial Infection Surveillance System rates]. / Estudio prospectivo de la infección nosocomial en una UCI médica. Una propuesta para el uso generalizado de las tasas del National Nosocomial Infection Surveillance System.

OBJECTIVE: To know the more relevant nosocomial infection (NI) rates in our Intensive Care Unit (ICU), risk factors associated with NI and trends in the infective flora. METHODS: During a three-month period, the cumulative incidence, density of overall incidence and device associated infection rates were determined in a total of 308 patients admitted to the medical ICU, following the recommendations of the National Nosocomial Infection Surveillance System (NNIS) in the USA. RESULTS: The cumulative incidence was 8.4 infections per 100 admissions. The density of overall incidence was 12.9 nosocomial infections per 1,000 days of ICU stay. Device-associated infection rates were: 28.9 pneumonia per 1,000 mechanical ventilation days, 5.3 urinary tract infections per 1,000 days of catheter use and 0.4 bacteremia per 1,000 days of central venous catheter. Pneumonia was the more common NI, followed by urinary tract infection. Pseudomonas aeruginosa was the microorganism recovered most frequently. The most common used antibiotics were third generation cephalosporins, followed by quinolones and macrolides. CONCLUSIONS: The use of NNIS rates is advisable because its allows to know the impact of NI on our unit and to perform comparative studies with other units of similar characteristics.

[High altitude retinal hemorrhages in the expeditions to 8,000 meter peaks. A study of 10 cases]. / Hemorragias retinianas en las expediciones a montañas de más de 8.000 m. Estudio de 10 casos.

BACKGROUND: Retinal haemorrhages are common at high altitude. Their pathogenesis is unknown. It has been suggested that they are less frequent in sherpas, and that possible predisposing factors might be the abscence of previous high-altitude experience, the extent of the high-altitude hypoxic exposure, polycythemia (because of hyperviscosity), history of cough and Valsalva manoeuvres during the expedition, existence of severe forms of mountain sickness (high-altitude pulmonary oedema and high-altitude cerebral oedema) and use of antiinflammatory drugs. The aim of this study is to know the incidence of retinal haemorrhages in the expeditions to mountains higher than 8.000 m and their relationship to the previously referred possible predisposing factors. SUBJECTS AND METHODS: Funduscopy was performed on 17 healthy subjects taking part in expeditions to Cho-Oyu (8.201 m) and to Shisha Pangma (8.046 m) and on six of their Nepali coworkers. RESULTS: Retinal haemorrhages were found in 10 of the European (59%) and in none of the Nepali mountaineers (p = 0.019). Other 2 Spanish climbers had tortuosity and engorgment of the retinal veins. No statistical association was found between retinal haemorrhages and maximal altitude attained prior to the expedition, maximal altitude reached during the present expedition, number of nights spent at extreme altitude, weight loss as an expression of chronic exposure to hypoxia, haemoglobin, history of cough or Valsalva manoeuvres during the expedition, existence of severe forms of mountain sickness or use of drugs. CONCLUSIONS: These results do not allow us to state that the mentioned factors predispose to high-altitude retinal haemorrhages.