The 2018 Lake Louise Acute Mountain Sickness Score.

Roach, Robert C., Peter H. Hackett, Oswald Oelz, Peter Bärtsch, Andrew M. Luks, Martin J. MacInnis, J. Kenneth Baillie, and The Lake Louise AMS Score Consensus Committee. The 2018 Lake Louise Acute Mountain Sickness Score. High Alt Med Biol 19:1-4, 2018.- The Lake Louise Acute Mountain Sickness (AMS) scoring system has been a useful research tool since first published in 1991. Recent studies have shown that disturbed sleep at altitude, one of the five symptoms scored for AMS, is more likely due to altitude hypoxia per se, and is not closely related to AMS. To address this issue, and also to evaluate the Lake Louise AMS score in light of decades of experience, experts in high altitude research undertook to revise the score. We here present an international consensus statement resulting from online discussions and meetings at the International Society of Mountain Medicine World Congress in Bolzano, Italy, in May 2014 and at the International Hypoxia Symposium in Lake Louise, Canada, in February 2015. The consensus group has revised the score to eliminate disturbed sleep as a questionnaire item, and has updated instructions for use of the score.

Intravenous thrombolysis for acute ischaemic stroke in a hospital without a specialised neuro-intensive care unit.

BACKGROUND: Treatment with intravenous (i.v.) recombinant tissue plasminogen activator (rt-PA) is recommended for selected patients with acute ischaemic stroke. We evaluated the feasibility and safety of this treatment in clinical practice in a hospital without a specialised neuro-intensive care unit. METHODS: We prospectively studied all patients who were treated with i.v. rt-PA for ischaemic stroke at our hospital between January 2001 and June 2002. The selection criteria corresponded to those published by the NINDS [1] and ECASS [2] groups. Time intervals between stroke symptom onset, hospital arrival and treatment with rt-PA were measured. A modified NIH stroke scale was used to assess clinical outcome 24 hours after stroke onset and before discharge. Cerebral computed tomography was performed prior to thrombolysis and again if the neurological status failed to improve or deteriorated. RESULTS: Thrombolytic therapy was administered to 15 acute ischaemic stroke patients, 13 men and two women with a median age of 69 years. The median time from stroke onset to rt-PA therapy was 135 minutes and from arrival in the emergency room to the start of thrombolysis 74 minutes. Ten patients exhibited early clinical improvement, defined as a decrease in NIHSS score by 4 points at 24 hours. Further improvement until discharge was observed in nine of these ten patients. One patient developed a non-fatal intracerebral haemorrhage. Another patient with severe stroke and clinical failure of thrombolysis died after 25 days. CONCLUSIONS: This study in a small patient population suggests that thrombolysis with rt-PA for acute ischaemic stroke is feasible without excess risk in a hospital experienced in the management of stroke patients, with a neurological consultant service but without a specialised neuro-intensive care unit (NICU). The outcome in this small series of patients corresponds to the results described in the randomised trials.

Characteristics of the ventilatory response in subjects susceptible to high altitude pulmonary edema during acute and prolonged hypoxia.

The present study compares the changes in ventilation in response to sustained hypobaric hypoxia and acute normobaric hypoxia between subjects susceptible to high altitude pulmonary edema (HAPE-S) and control subjects (C-S). Seven HAPE-S and five C-S were exposed to simulated high altitude of 4000 m for 23 h in a hypobaric chamber. Resting minute ventilation (V(E)), tidal volume (V(T)), and respiratory frequency (f(R)), as well as the end-tidal partial pressures of oxygen (P(ET(O2))) and carbon dioxide (P(ET(CO2))) were measured in all subjects sitting in a standardized position. Six measurement periods were recorded: ZH1 at 450 m at Zurich level, HA1 on attaining 3600 m altitude, HA2 after 20 min at 4000 m, HA3 after 21 h and HA4 after 23 h at 4000 m altitude, and ZH2 immediately after recompression to Zurich level. At ZH1 and HA3, the measurements were first done in lying, then in sitting, and afterwards in standing. Peripheral arterial oxygen saturation (Sa(O2)) was continuously recorded. All respiratory parameters were also measured during exercise lasting 30 min, the work load being 50% of maximal oxygen consumption (V(O2max)) at Zurich level and 26% of the Zurich V(O2max) at 4000 m. V(E), P(ET(O2)) and P(ET(CO2)) did not significantly differ between HAPE-S and C-S at rest and during exercise periods at Zurich level and at high altitude. However, Sa(O2) was significantly lower in HAPE-S than in C-S at rest and during exercise at 4000 m. Breathing through the mouthpiece during ventilation measurements increased significantly the Sa(O2) in HAPE-S in posture tests at HA3. This effect was most pronounced in the supine posture, in which HAPE-S had the lowest Sa(O2) values. These data provide evidence that (1) gas exchange might be impaired on the level of ventilation-perfusion mismatch or due to diffusion limitation in HAPE-S during the first 23 h of exposure to a simulated altitude of 4000 m, and (2) contrary to C-S, the Sa(O2) in HAPE-S is significantly affected by body position and by mouthpiece breathing.