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A 36-year-old woman with no medical history participated in a trekking in Ladakh up to 5300 m of altitude. She was well acclimatized and presented no previous sign of acute mountain sickness, high altitude pulmonary edema or high altitude cerebral edema. After an intense effort to catch up with her group, she became breathless and complained of visual disturbances, fatigue, dizziness, and confusion. During her descent to a lower altitude (4800 m), with the help of companions, she lost consciousness several times. After a 14-hour sleep, she recovered and all symptoms disappeared so that she was able to walk along with the group for 20 km. On returning home, she went through a battery of examinations that were all normal: cerebral magnetic resonance imaging, Doppler of supra-aortic arteries, 24 hours Holter, and cardiac transthoracic and transesophageal echography. A hypoxia exercise test revealed a hyper-response to hypoxia with severe hypocapnia. The etiology of this neurological episode is discussed (transient embolic ischemic attack, migraine, cerebral edema, and global amnesia). The patchy distribution of neurological symptoms is not in favor of a thrombotic event. The most probable diagnosis proposed is a transient cerebral ischemia due to local cerebral vasoconstriction related to hyperventilation-induced hypocapnia in a context of acute severe exercise. Special attention should be given to subjects who show a hyper-responsiveness to hypoxia before a sojourn at high altitude: they should avoid unnecessary hyperventilation due to any kind of stress, emotion, or exhaustive exercise.

We evaluated the benefits of on-demand systematic screening for Chlamydia trachomatis and Neisseria gonorrhoeae using the Xpert CT/NG assay in 589 women attending family planning clinics. The sexually transmitted infection prevalence was 16.5% with 15.1% C. trachomatis and 3.1% N. gonorrhoeae infections. The on-demand test allowed for a quicker management of patients at high risk for sexually transmitted infections.

BackgroundRisk prediction of acute mountain sickness, high altitude (HA) pulmonary or cerebral edema is currently based on clinical assessment. Our objective was to develop a risk prediction score of Severe High Altitude Illness (SHAI) combining clinical and physiological factors. Study population was 1017 sea-level subjects who performed a hypoxia exercise test before a stay at HA. The outcome was the occurrence of SHAI during HA exposure. Two scores were built, according to the presence (PRE, n = 537) or absence (ABS, n = 480) of previous experience at HA, using multivariate logistic regression. Calibration was evaluated by Hosmer-Lemeshow chisquare test and discrimination by Area Under ROC Curve (AUC) and Net Reclassification Index (NRI).ResultsThe score was a linear combination of history of SHAI, ventilatory and cardiac response to hypoxia at exercise, speed of ascent, desaturation during hypoxic exercise, history of migraine, geographical location, female sex, age under 46 and regular physical activity. In the PRE/ABS groups, the score ranged from 0 to 12/10, a cut-off of 5/5.5 gave a sensitivity of 87%/87% and a specificity of 82%/73%. Adding physiological variables via the hypoxic exercise test improved the discrimination ability of the models: AUC increased by 7% to 0.91 (95%CI: 0.87-0.93) and 17% to 0.89 (95%CI: 0.85-0.91), NRI was 30% and 54% in the PRE and ABS groups respectively. A score computed with ten clinical, environmental and physiological factors accurately predicted the risk of SHAI in a large cohort of sea-level residents visiting HA regions.

A 45-year-old healthy man wishes to climb Mount Kilimanjaro (5895 m) in a 5-day period, starting at 1800 m. The results of a recent exercise stress test were normal; he runs 10 km 4 or 5 times per week and finished a marathon in less than 4 hours last year. He wants to know how he can prevent becoming ill at high altitude and whether training or sleeping under normobaric hypoxic conditions in the weeks before the ascent would be helpful. What would you advise?

A 24-year-old adult with a Down syndrome was admitted in December 2006 at the Moutiers hospital in the French Alps for an acute inaugural episode of high altitude pulmonary edema (HAPE) that occurred in the early morning of day 3 after his arrival to La Plagne (2000 m). This patient presented an interventricular septal defect operated on at the age of 7, a hypothyroidism controlled by 50 microg levothyrox, a state of obesity (BMI 37.8 kg/m(2)), and obstructive sleep apneas with a mean of 42 obstructive apneas or hypopneas per hour, treated with continuous positive airway pressure (CPAP). The patient refused to use his CPAP during his stay in La Plagne. At echocardiography, resting parameters were normal, with a left ventricular, ejection fraction of 60%, a normokinetic right ventricle, and an estimated systolic pulmonary artery pressure (sPAP) of 30 mmHg. At exercise, sPAP rose to 45 mmHg and the right ventricle was still normokinetic and not dilated. An exercise hypoxic tolerance test performed at 60 W and at the equivalent altitude of 3300 m revealed a severe drop in arterial oxygen saturation down to 60%, with an abnormal low ventilatory response to hypoxia, suggesting a defect in peripheral chemosensitivity to hypoxia. In conclusion, patients with Down syndrome, including adults with no cardiac dysfunction and regular physical activity, are at risk of HAPE even at moderate altitude when they suffer from obstructive sleep apneas associated with obesity and low chemoresponsiveness. This observation might be of importance since an increasing number of young adults with Down syndrome participate in recreational or sport activities, including skiing and mountaineering.

To the Editor: Anaphylactic reactions are a common complication of anesthesia, most often related to the use of muscle relaxants.1 The intensity varies from mild clinical manifestations to severe anaphylactic shock and death.2 With increased public awareness and the improvement in the detection and diagnosis of such adverse events, an increased frequency has been reported in most developed countries.3 In France, a recent survey estimated the incidence of anaphylactic reactions to be as high as one amongst 6,500 anesthetic procedures when a muscle relaxant is used.1 Approximately four individuals per 100 population (2.5 million) receive muscle relaxants during anesthesia every year.4 These data allow us to postulate that among the French population alone (60 million people), 350 patients every year will develop a muscle relaxant mediated anaphylactic reaction. Similarly, thousands of patients all over the world will experience similar adverse events. Risk reduction requires that the use of muscle relaxants be limited inasmuch as possible since anaphylaxis may occur in patients with or without a previous history of allergy.1 To date, there are two main indications for muscle relaxants during anesthesia for elective surgery. The first involves the anesthetic procedure itself, i.e., tracheal intubation, while the second relates to the surgical procedure. Muscular relaxation facilitates airway management, access to the surgical site, closure of the abdominal wall and avoids inopportune movements. However, muscle relaxants are no longer mandatory. There is now evidence that the development of new hypnotic drugs has changed airway management and allows tracheal intubation without the need for muscle relaxants in a selected population.5 From a surgical point of view, abdominal and thoracic procedures usually require muscular relaxation but, on the other hand, numerous peripheral surgical procedures such as lower abdominal and limb operations do not require the use of curare. While recent data show that it is possible to intubate the trachea without resorting to muscle relaxants, the topic remains controversial. Intubating habits vary both locally and internationally. It has been suggested that muscle relaxants decrease pharyngeal and laryngeal trauma secondary to intubation.5 As a result, several anesthesiologists are reluctant to curtail muscle relaxation for intubation. In 1996, in France, only 16% of anesthetics requiring tracheal intubation were conducted without the use of muscle relaxants.4 This puts us in a delicate situation. As anesthesiologists, we use a class of drugs, muscle relaxants, known to mediate anaphylaxis with potentially lifethreatening consequences whereas, on the other hand, there is no more doubt that we are able to avoid these drugs in many situations. Should we still widely use muscle relaxants or should we restrict their prescription? Patient safety during anesthesia requires us to take into account all risks, even those that may have been underestimated in the past.

Disruption of a mainstem bronchus is a rare but dreaded complication of pneumonectomy. After an anatomic study on cadavers, we successfully used a video mediastinoscope to close a postpneumonectomy main bronchus fistula via a cervical incision.

Haemostasis has been studied by several authors during exposure to altitude hypoxia. On acute induction to hypoxia, platelet count, platelet aggregability and bleeding time are normal; an increase of thromboxane released from platelets and of prostacyclin, released from endothelial cells is observed; coagulation factors are unchanged except of F. VIII which is increased; modified antithrombin III (ATm) are normal; fibrinopeptide A is increased in subjects with pulmonary edema and fibrinolytic activity after venous occlusion is normal. In chronic hypoxia, during a stay at 6542 m (Mt. Sajama), we found in 7 subjects an important increase in D. Dimer (p < 0.001) that seems to correspond to an activation of coagulation and a decrease of F. VIII R. Cof/F. VIII R. Ag ratio which suggests an endothelial cell damage.