Environmental Symptoms Questionnaire Research Articles

Nocturnal periodic breathing and arterial oxygen desaturation in acute mountain sickness

The objective of this case-control study was to investigate the relationship between periodic breathing (PB) and acute mountain sickness (AMS). Nine volunteers, healthy lowlanders between the age of 20 and 36 years stayed at a simulated altitude of 3700 m (485 Torr) for 24 h in a hypobaric chamber. A sleep study was carried out for more than 6 h. Arterial oxygen saturation (SaO2) was monitored by finger oximetry on all subjects. PB was determined by a polysomnography (EEG, EOG, thoracic movement) in six subjects and was indirectly measured by studying the cyclic change of SaO2 in three other subjects. The severity of AMS was assessed with the Environmental Symptoms Questionnaire. All subjects showed lower SaO2 during sleep than when awake (65.0 ± 6.4% versus 72.6 ± 6.4%, p < 0.01), and symptoms of AMS were more intense the next morning. PB was observed in eight of the nine subjects; however, the time spent in PB (%PB) ranged from 0% to 57.8%. There was a positive correlation between %PB and stage 1 sleep, suggesting an important role of PB in poor sleep quality at high altitude. Percent PB, however, was not significantly correlated with the degree of sleep desaturation, the severity of AMS, and ventilatory responses to hypoxia and hypercapnia. These results suggest that PB may not be a critical factor for sleep desaturation and in the development of AMS for high-altitude newcomers.

Dexamethasone for prophylaxis against acute mountain sickness during rapid ascent to 5334 m

Twenty-three volunteers participated in a double-blind, randomized trial comparing the steroid dexamethasone 4 mg to placebo every 12 h as prophylaxis against acute mountain sickness (AMS) during a rapid ascent to a shelter on Mt Chaclataya, Bolivia. From sea level, subjects were transported by air and land vehicles to 5334 m within a 72-h period. They were evaluated by cerebral scores derived from the Environmental Symptom Questionnaire and confirmed by AMS-C and AMS-R scores. After 6–8 h at high altitude (day 3), the number of ill persons in the dexamethasone group was less than those ill in the placebo group (χ2 = 7.43, p = 0.01) by chi-square and Fisher's exact tests. After 20 h at high altitude (day 4), the contrast between groups diminished (χ2 = 2.10, p = 0.214). ANOVA and t-test showed that mean cumulative AMS scores of the dexamethasone group were significantly lower ( p = 0.01, p = 0.02) than those of the placebo group for both days at high altitude, despite an approximate 82% increase in the mean cumulative score of the dexamethasone group from day 3 to day 4. We conclude that dexamethasone 4 mg every 12 h, though initially effective, was not sufficient to sustain prophylaxis from AMS symptoms at 5334 m.

Associations between mood and specific health composites during U.S. Navy Persian Gulf operations

Previously conducted field studies using shipboard U.S. Navy personnel during at-sea operations in the Persian Gulf have shown that crew members experience mood changes and degradations in general physical health. The objectives of this study were to: (a) examine the relationship between mood and health complaints among personnel deployed in the Persian Gulf; and (b) extend previous research using specific health composites rather than a general measure of health. Mood was assessed for 104 shipboard volunteers using the Profile of Mood States Tension/Anxiety and Fatigue subscales. Health symptoms were measures using the Environmental Symptoms Questionnaire. Results of multiple regression analyses showed that each of 11 distinct health composites was significantly associated with one or both mood variables. Further, the two mood factors were differentially associated with 9 of the 11 health composites. This study underscores the usefulness of employing multiple specific health measures rather than global measures.

Pulmonary Function and Hypoxic Ventilatory Response in Subjects Susceptible to High-Altitude Pulmonary Edema

To determine if spirometric changes reflect early high-altitude pulmonary edema (HAPE) formation, we measured the FVC, FEV1, and FEF25-75 serially during the short-term period following simulated altitude exposure (4,400 m) in eight male subjects, four with a history of HAPE and four control subjects who had never experienced HAPE. Three of the four HAPE-susceptible subjects developed acute mountain sickness (AMS), based on their positive Environmental Symptom Questionnaire (AMS-C) scores. Clinical signs and symptoms of mild pulmonary edema developed in two of the three subjects with AMS after 4 h of exposure, which prompted their removal from the chamber. Their spirometry showed small decreases in FVC and greater decreases in FEV1 and FEF25-75 after arrival at high altitude in the presence of rales or wheezing on clinical examination and normal chest radiographs. One of the two subjects had desaturation (59 percent) and tachycardia during mild exercise, and excessive fatigue and inability to complete the exercise protocol developed in the other at 4 h. The six other subjects had minimal changes in spirometry and did not develop signs of lung edema. Further, we measured each subject's ventilatory response to hypoxia (HVR) prior to decompression to determine whether the HVR would predict the development of altitude illness in susceptible subjects. In contrast to anticipated results, high ventilatory responses to acute hypoxia, supported by increased ventilation during exposure to high altitude, occurred in the two subjects in whom symptoms of HAPE developed. The results confirm that HAPE can occur in susceptible individuals despite the presence of a normal or high ventilatory response to hypoxia.

High altitude pulmonary edema after successful treatment of acute mountain sickness with dexamethasone

Case report A 28-year-old previously healthy male mountaineer with a history of radiologically documented HAPE participated in a study conducted in the high altitude research laboratory of the Capanna Margherita (4559 m) in the Alps Valais. The results of this study have been reported in detail elsewhere [8-10]. The subject had ascended from 1170 to 4559 m within a 24 h period, starting the ascent on foot at 3220 m and staying overnight at 3611 m. After the first night spent at 4559 m, he presented with severe AMS manifested by headache resistant to acetaminophen, nausea, insomnia, lassitude and dizziness. Clinical examination revealed facial edema, rales dorsally over the right middle lung field, no neurological abnormalities and normal fundoscopy. The severity of AMS was assessed by the environmental symptom questionnaire (ESQ) [11], which suggests a criterion score of > 0.70 for the subscore AMS-C reflecting cerebral symptoms and> 0.60 for the subscore AMS-R reflecting respiratory symptoms. The scores of AMS-C and AMS-R were 2.08 and 1.39, respectively, in this patient. The postero-anterior chest X-ray at this time showed no evidence of interstitial or alveolar pulmonary edema (Fig. lA). The patient was treated orally with 8 mg dexamethasone at 8 a.m. and 4 mg at 4 p.m. Thereafter, treatment was discontinued because of recovery from AMS symptoms in the evening with AMS-C and AMS-R scores of 0.68 and 0.44, respectively. At 6 a.m. on the following day, he presented with the same symptoms and clinical findings as 24 h previously, with scores of 2.46 (AMS-C) and 0.68 (AMS-R). The chest radiograph now

The Effect of Naproxen on Acute Mountain Sickness and Vascular Responses to Hypoxia

The role of prostaglandins in the pathogenesis of acute mountain sickness and two hypoxia-induced vascular responses was evaluated using the cyclooxygenase inhibitor naproxen. Eleven men spent 24 hours at sea level, followed by 34 hours of decompression to 428 mm Hg while receiving naproxen (N), 250 mg twice daily or placebo (P) in a double-blind crossover trial. Serum naproxen levels measured by high pressure liquid chromatography were not changed by hypoxia. The severity of acute mountain sickness (AMS) by the Environmental Symptom Questionnaire scores and observer assessment were unaffected by drug treatment. Retinal artery diameter measured from projected fundus photographs was increased after 27 hours at altitude (11.4 +/- .5 mm) vs. sea level (9.4 +/- .5 mm, p less than 0.05) during both trials. Upright mean arterial pressure fell after 6 hours at altitude (79 +/- 3 mm Hg during N and P vs. 92 +/- 3 at sea level, p less than 0.01). Minute ventilation, end expiratory alveolar PO2 and PCO2 did not differ between drug trials. This study suggests vasodilating prostaglandins do not have a major role in the genesis of AMS, hypoxia-induced retinal vasodilatation, or postural blood pressure responses in man.