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High Altitude Edema

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181. Exercise Testing, Supplemental Oxygen and Hypoxia. (PubMed)

in such patients is lacking. CPET performance with supplemental O2 in respiratory patients residing at high altitudes is also poorly studied. Finally, CPET has the potential to give physiological and clinical information about acute and chronic mountain sickness, high-altitude pulmonary edema, and high-altitude cerebral edema. It may also translate high-altitude acclimatization and adaptive processes in healthy individuals into intensive care medical practice. (...) peak [Formula: see text]o2, care should be taken in the selection of work-rate incrementation rates when CPET performance is to be compared with normobaria at sea level. CPET has been used to evaluate the effects of supplemental O2 on exercise intolerance in chronic obstructive pulmonary disease, interstitial pulmonary fibrosis, and cystic fibrosis at sea level. However, identification of those CPET indices likely to be predictive of supplemental O2 outcomes for exercise tolerance at altitude

2017 Annals of the American Thoracic Society

182. Association between genetic polymorphism of telomere-associated gene ACYP2 and the risk of HAPE among the Chinese Han population: A Case-control study. (PubMed)

Association between genetic polymorphism of telomere-associated gene ACYP2 and the risk of HAPE among the Chinese Han population: A Case-control study. High-altitude pulmonary edema (HAPE) is a hypoxia-induced, life-threatening, pulmonary edema, which is characterized by exaggerated pulmonary hypertension caused by stress failure. ACYP2 was found to associated with telomere length, the aim of this study was to identify whether ACYP2 polymorphisms increase or decrease HAPE risk in the Chinese

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2017 Medicine

183. Magnetic Resonance Spectroscopy Studies of Acute Hypoxic and Hyperoxic Breathing in Healthy Volunteers

endanger the subject during or after a blood draw (e.g. hemophilia) Significant medical or neurological illness Prior high altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE) diagnosis Born at altitudes greater than 2,100 m (~7,000 ft) Systemic disease with or without any functional limitation; including controlled hypertension controlled diabetes without systemic effects any cardiac conditions with or without functional limitation, such as, coronary artery disease or valve disease

2017 Clinical Trials

184. A Signature of Circulating microRNAs Predicts the Susceptibility of Acute Mountain Sickness (PubMed)

A Signature of Circulating microRNAs Predicts the Susceptibility of Acute Mountain Sickness Background: Acute mountain sickness (AMS) is a common disabling condition in individuals experiencing high altitudes, which may progress to life-threatening high altitude cerebral edema. Today, no established biomarkers are available for prediction the susceptibility of AMS. MicroRNAs emerge as promising sensitive and specific biomarkers for a variety of diseases. Thus, we sought to identify circulating (...) microRNAs suitable for prediction the susceptible of AMS before exposure to high altitude. Methods: We enrolled 109 healthy man adults and collected blood samples before their exposure to high altitude. Then we took them to an elevation of 3648 m for 5 days. Circulating microRNAs expression was measured by microarray and quantitative reverse-transcription polymerase chain reaction (qRT-PCR). AMS was defined as Lake Louise score ≥3 and headache using Lake Louise Acute Mountain Sickness Scoring System

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2017 Frontiers in physiology

185. IL-10 Dysregulation in Acute Mountain Sickness Revealed by Transcriptome Analysis (PubMed)

IL-10 Dysregulation in Acute Mountain Sickness Revealed by Transcriptome Analysis Acute mountain sickness (AMS), which may progress to life-threatening high-altitude cerebral edema, is a major threat to millions of people who live in or travel to high altitude. Although studies have revealed the risk factors and pathophysiology theories of AMS, the molecular mechanisms of it do not comprehensively illustrate. Here, we used a system-level methodology, RNA sequencing, to explore the molecular (...) mechanisms of AMS at genome-wide level in 10 individuals. After exposure to high altitude, a total of 1,164 and 1,322 differentially expressed transcripts were identified in AMS and non-AMS groups, respectively. Among them, only 328 common transcripts presented between the two groups. Immune and inflammatory responses were overrepresented in participants with AMS, but not in non-AMS individuals. Anti-inflammatory cytokine IL10 and inflammation cytokines IF17F and CCL8 exhibited significantly different

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2017 Frontiers in immunology

186. Chronic Hypobaric Hypoxia Modulates Primary Cilia Differently in Adult and Fetal Ovine Kidneys (PubMed)

Chronic Hypobaric Hypoxia Modulates Primary Cilia Differently in Adult and Fetal Ovine Kidneys Hypoxic environments at high altitude have significant effects on kidney injury. Following injury, renal primary cilia display length alterations. Primary cilia are mechanosensory organelles that regulate tubular architecture. The effect of hypoxia on cilia length is still controversial in cultured cells, and no corresponding in vivo study exists. Using fetal and adult sheep, we here study the effect (...) of chronic hypobaric hypoxia on the renal injury, intracellular calcium signaling and the relationship between cilia length and cilia function. Our results show that although long-term hypoxia induces renal fibrosis in both fetal and adult kidneys, fetal kidneys are more susceptible to hypoxia-induced renal injury. Unlike hypoxic adult kidneys, hypoxic fetal kidneys are characterized by interstitial edema, tubular disparition and atrophy. We also noted that there is an increase in the cilia length

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2017 Frontiers in physiology

187. Acute Rhinosinusitis in Adults

, foreign body); mucosal edema (rhinitis: allergic, vasomotor, viral); rapid change in altitude or pressure; impaired ciliary motility (Kartagener’s syndrome, cystic fibrosis, and smoking); dental infections and immunodeficiency (HIV, immunoglobulin deficiencies). Probability estimation. The probability of acute bacterial rhinosinusitis can be estimated based on history and physical exam. The signs and symptoms found most likely to predict rhinosinusitis are given in Tables 1 and 3. Williams, et al (...) be justified. Likely to be effective in treating symptoms. • Topical steroids reduce edema and inflammation and may improve symptoms in acute rhinosinusitis. Studies have not clearly demonstrated a benefit in any role other than symptom management. Expert opinion suggests that high dose nasal steroids are most likely to be effective. • Topical decongestants may decrease nasal congestion; expert opinion suggests that they may improve drainage. Topical decongestant use should be limited to 3 days due

2013 University of Michigan Health System

188. 2012 KDIGO Clinical Practice Guideline for the Evaluation and Management of CKD

(in mg/l), min indicates the minimum of SCysC/0.8 or 1, and max indicates the maximum of SCysC/0.8 or 1. Grade Quality of evidence Meaning A High We are confident that the true effect lies close to that of the estimate of the effect. B Moderate The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different. C Low The true effect may be substantially different from the estimate of the effect. D Very low The estimate of effect is very (...) / 1.73 m 2 ) Description and range G1 Normal or high =90 G2 Mildly decreased 60-89 G3a Mildly to moderately decreased 45-59 G3b Moderately to severely decreased 30-44 G4 Severely decreased 15-29 G5 Kidney failure 300 mg/g >30 mg/mmol GFR categories (ml/min/ 1.73 m 2 ) Description and range G1 Normal or high =90 G2 Mildly decreased 60-89 G3a Mildly to moderately decreased 45-59 G3b Moderately to severely decreased 30-44 G4 Severely decreased 15-29 G5 Kidney failure 300 mg/g >30mg/mmol GFR

2012 National Kidney Foundation

189. Management of Pulmonary Arterial Hypertension

hypoventilation disorders 3.6. Chronic exposure to high altitude 3.7. Developmental abnormalities 4. Chronic thromboembolic pulmonary hypertension (CTEPH) 5. Pulmonary hypertension with unclear multifactorial mechanisms 5.1. Haematologic disorders: myeloproliferative disorders, splenectomy 5.2. Systemic disorders: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis 5.3. Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid disorders (...) resistance (PVR) with progression to right-sided heart failure and ultimately death. 1 Mortality rates in patients with PAH are high: historically, the median life expectancy of idiopathic PAH (IPAH) without specific therapy is 2.8 years from diagnosis, with 1-year, 3-year, and 5-year survival rates of 68%, 48% and 34%, respectively. 2 In addition, most patients with PAH have a compromised quality of life (QoL) with limited physical activity and social function. 3 With our rapidly evolving knowledge

2011 Ministry of Health, Malaysia

190. Multiparametric Magnetic Resonance Investigation of Brain Adaptations to 6 Days at 4350 m (PubMed)

Multiparametric Magnetic Resonance Investigation of Brain Adaptations to 6 Days at 4350 m Hypoxic exposure in healthy subjects can induce acute mountain sickness including headache, lethargy, cerebral dysfunction, and substantial cerebral structural alterations which, in worst case, can lead to potentially fatal high altitude cerebral edema. Within this context, the relationships between high altitude-induced cerebral edema, changes in cerebral perfusion, increased brain parenchyma volume (...) matter alterations after several days at high altitude when subjects are asymptomatic that may represent the normal brain response to prolonged high altitude exposure.

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2016 Frontiers in physiology

191. Prolonged Hypoxic Breathing in Healthy Volunteers: a Safety Study

for Study: 18 Years to 40 Years (Adult) Sexes Eligible for Study: All Accepts Healthy Volunteers: Yes Criteria Inclusion criteria Have a photo identification (ID) Male or female individuals age between 18 and 40 years old BMI between 19 and 24.9 kg/m2 Having capacity to consent to the study Exclusion criteria Evidence of any physical, mental, and/or medical conditions that would make the proposed studies relatively more hazardous Prior high altitude pulmonary edema (HAPE) or high-altitude cerebral edema (...) ) between 80%-85% (corresponding to 40-55 mmHg of arterial partial oxygen pressure (PaO2)). Healthy volunteers will be monitored and blood and urine will be obtained at 24h and 48 hours after returning to normoxia. Other: Inhaled Nitrogen To create the correct gas mixture, nitrogen tanks or membrane technology nitrogen generators will be utilized. Humidified, high flow, hypoxic gas by nasal cannula will allow the participant to walk short distances, eat, execute basic personal needs (e.g., use

2016 Clinical Trials

192. Controlled Hyperventilation as Prophylaxis for Acute Mountain Sickness

30 days BMI> 30 Pharmaceutical use as diuretics, corticosteroids, acetazolamide, or anti -inflammatory drugs during the 2 weeks prior to the study A history of high altitude cerebral edema or high altitude pulmonary edema Cardiovascular risk factors such as a personal history of cardiovascular disease, familial history of major adverse cardiovascular events (MACE) at age younger than 45 yrs, hypercholesterolemia and stroke. Contacts and Locations Go to Information from the National Library (...) Voluntary increase in respiration Behavioral: Voluntary ventilatory response Training of the subjects for voluntary increase in the respiratory minute ventilation Active Comparator: Acetazolamide Administration of Acetazolamide 125mg. since 24 hours before ascent and until 48 hours post altitude exposure, and absence of altitude sickness symptoms Drug: Acetazolamide Acetazolamide 125mg. PO every 12 hours since 24 hours before ascent, until 48 hours at high altitude Outcome Measures Go to Primary Outcome

2016 Clinical Trials

193. Effect of Hypoxia on Cognitive Assessment and Cerebral Activity in Healthy Volunteers

or psychotropic drugs or substances BMI inferior to 25 Kg/m2 French speaker and able to understand the test instructions Informed consent form signed Exclusion Criteria: Subject with history or current brain disease (severe brain trauma, transient ischemic attack, stroke, epilepsy, cerebral tumor…) or retinal pathologies (including familial DMLA) Subject with history of Acute Mountain Sickness, High Altitude Cerebral Edema or High Altitude Pulmonary Edema Subject with other major medical or surgical history

2016 Clinical Trials

194. Biomarkers of hypoxia, endothelial and circulatory dysfunction among climbers in Nepal with AMS and HAPE: a prospective case-control study. (PubMed)

Biomarkers of hypoxia, endothelial and circulatory dysfunction among climbers in Nepal with AMS and HAPE: a prospective case-control study. The mechanisms underlying acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) are not fully understood. We hypothesized that regulators of endothelial function, circulatory homeostasis, hypoxia and cell stress contribute to the pathobiology of AMS and HAPE.We conducted a prospective case-control study of climbers developing altitude (...) compared to AC or AMS. ET-1 levels were associated with disease severity as indicated by oxygen saturation. Angiopoietin-like 4 (Angptl4) and resistin, a marker of cell stress, were associated with AMS and HAPE irrespective of severity. Corin and angiotensin converting enzyme, regulators of volume homeostasis, were significantly decreased in HAPE compared to AC.Our findings indicate that regulators of endothelial function, vascular tone and cell stress are altered in altitude illness and may

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2016 Journal of Travel Medicine

195. Painless acute myocardial infarction on Mount Kilimanjaro (PubMed)

Painless acute myocardial infarction on Mount Kilimanjaro An individual experiencing dyspnoea or syncope at high altitude is commonly diagnosed to have high-altitude pulmonary edema or cerebral edema. Acute myocardial infarction (AMI) is generally not considered in the differential diagnosis. There have been very rare cases of AMI reported only from Mount Everest. We report a case of painless ST segment elevation myocardial infarction (STEMI) that occurred while climbing Mount Kilimanjaro. A 51 (...) -year-old man suffered dyspnoea and loss of consciousness near the mountain peak, at about 5600 m. At a nearby hospital, he was treated as a case of high-altitude pulmonary edema. ECG was not obtained. Two days after the incident, he presented to our institution with continued symptoms of dyspnoea, light-headedness and weakness, but no pain. He was found to have inferior wall and right ventricular STEMI complicated by complete heart block. He was successfully managed with coronary angioplasty

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2016 BMJ case reports

196. Neuroprotective Role of Intermittent Hypobaric Hypoxia in Unpredictable Chronic Mild Stress Induced Depression in Rats (PubMed)

Neuroprotective Role of Intermittent Hypobaric Hypoxia in Unpredictable Chronic Mild Stress Induced Depression in Rats Hypoxic exposure results in several pathophysiological conditions associated with nervous system, these include acute and chronic mountain sickness, loss of memory, and high altitude cerebral edema. Previous reports have also suggested the role of hypoxia in pathogenesis of depression and related psychological conditions. On the other hand, sub lethal intermittent hypoxic (...) elevated plus maze (EPM), open field test (OFT), force swim test (FST), as behavioural paradigm and related histological and molecular approaches. The data indicated the UCMS induced depression like behaviour as evident from decreased exploration activity in OFT with increased anxiety levels in EPM, and increased immobility time in the FST; whereas on providing the IHH (5000m altitude, 4hrs/day for two weeks) these behavioural changes were ameliorated. The morphological and molecular studies also

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2016 PloS one

197. Dyspnea Causes

, Causes of Dyspnea with Clear Lung Sounds From Related Chapters II. Causes: Categories of Dyspnea Oxygen Ingress problem High altitude Airway Obstruction or trachea (e.g. , ) (e.g. , ) Alveoli (e.g. , ) External compression (e.g. ) Thoracic wall (e.g. ) Oxygen Uptake problem circulation (left side) disorder (oxygen carrying capacity) Neuromuscular problem Miscellaneous causes Perceived (e.g. anxiety) (with compensatory ) III. Causes: Common in Adults in Adults (Mnemonic: PPOPPA) Pulmonary edema (...) Pulmonary: Noxious gas inhalation, Cardiogenic: Obstructed Airway (Foreign body, ) (Spontaneous) or in Adults (Duration >1 month) ( , ) Kyphoscoliosis Neuromuscular disease (e.g. ) Upper airway conditions Psychiatric cause (e.g. ) IV. Causes: Dyspnea with Clear Lung Sounds Observe for signs of right (edema, JVD) V. Causes: Acute Dyspnea in Children VI. Causes: Airway Causes VII. Causes: Cardiac Causes ( ) Asymmetric septal hypertrophy Valvular dysfunction (e.g. ) Arrhythmias (e.g. ) VIII. Causes

2018 FP Notebook

198. Frostbite

Chapters II. Definitions Frostbite Skin (and deeper structures) freeze resulting in tissue injury Frostnip Superficial ice crystals deposit on the skin surface without tissue injury III. Risk Factors (e.g. ) Prolonged cold or moisture exposure High wind (high wind chill) High altitude Inadequate clothing Extremes of age strictive agents (e.g. nicotine) IV. Pathophysiology: Changes by skin Temperature Room Normal skin perfusion >200 ml/min Skin 59 F (15 C) Skin perfusion 20-50 ml/min striction (...) bullae Fourth-degree Frostbite (full skin thickness AND muscle/bone involvement) Mottled, deep red or cyanotic skin Bone and muscle freezing Dry , black mummified skin VII. Signs: Classification - 2 category (preferred in the acute setting) Distribution - high risk areas Extremities (hands, feet) Face (ears, nose) Genitalia (penis) Superficial Frostbite (includes first and second degree Frostbite as above) Erythema and edema Minimal to no tissue loss No hemorrhagic bullae (but clear or milky bullae

2018 FP Notebook

199. Respiratory Alkalosis

Alkalosis Aka: Respiratory Alkalosis II. Causes Increased Central Respiratory Drive Anxiety Medications s Nicotine s (especially with ) Pregnancy failure, or Increased Chemoreceptor Stimulation Pulmonary edema High altitude (decreased FIO2) (early) Iatrogenic with III. Labs Arterial pH increased Serum bicarbonate decreased decreased Acute Respiratory Alkalosis decreases by 10 mmHg increases pH by 0.08 Bicarbonate decreases 2 meq/L per 10 mmHg fall Chronic Respiratory Alkalosis decrease by 10 mmHg

2018 FP Notebook

200. Hypoxia

or Hypoxemia <70 to 80 mmHg III. Causes Pulmonary edema ( ) Acute ic Hypersensitivity pneumonitis ( ) Miscellaneous Causes Decreased FIO2 of inspired air (high altitude) Cyanide IV. Causes: Hypoxia or Hypoxemia (PaO2 <70 to 80 mmHg) See Hypoxemia V. Symptoms VI. Signs Mental status changes Acute: Chronic: , drowsy, inattentive ( ) decreased Usually correlates with However, relationship is not linear (See ) Not sensitive for increased Conditions where low despite normal or other abnormal VII. Evaluation

2018 FP Notebook

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