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In order to reduce intradialytic and interdialytic morbidity, it is important to obtain a zero sodium balance at the end of each dialysis session. This can be achieved by matching exactly the interdialytic sodium and water intake with the intradialytic sodium and water removal. A positive sodium balance can be obtained by using hypernatric dialysis or "sodium ramping" or convective techniques. While reducing the intradialytic side effects (hypotension, cramps, nausea, vomiting), these methods may increase the interdialytic side effects (thirst, weight gain, hypertension and pulmonary edema). Given the highly variable amounts of sodium introduced during the interdialytic periods, the use of sodium-conductivity kinetic models allows removing exactly the amount of sodium accumulated in the interdialytic period. This strategy may be advantageous towards cardiovascular stability in patients prone to dialysis hypotension.
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PMID:Sodium balance during extra corporeal dialysis. 1820 81

The key elements in acclimatization aim at securing the oxygen supply to tissues and organs of the body with an optimal oxygen tension of the arterial blood. In acute exposure, ventilation and heart rate are elevated with a minimum reduction in stroke volume. In addition, plasma volume is reduced over 24-48 h to improve the oxygen-carrying capacity of the blood, and is further improved during a prolonged sojourn at altitude through an enhanced erythropoiesis and larger Hb mass, allowing for a partial or full restoration of the blood volume and arterial oxygen content. Most of these adaptations are observed from quite low altitudes [approximately 1000 m above sea level (m a.s.l.)] and become prominent from 2000 m a.s.l. At these higher altitudes additional adaptations occur, one being a reduction in the maximal heart rate response and consequently a lower peak cardiac output. Thus, in spite of a normalization of the arterial oxygen content after 4 or more weeks at altitude, the peak oxygen uptake reached after a long acclimatization period is essentially unaltered compared with acute exposure. What is gained is a more complete oxygenation of the blood in the lungs, i.e. SaO(2) is increased. The alteration at the muscle level at altitude is minor and so is the effect on the metabolism, although it is debated whether a possible reduction in blood lactate accumulation occurs during exercise at altitude. Transient acute mountain sickness (headache, anorexia, and nausea) is present in 10-30% of subjects at altitudes between 2500 and 3000 m a.s.l. Pulmonary edema is rarely seen below 3000 m a.s.l. and brain edema is not seen below 4000 m a.s.l. It is possible to travel to altitudes of 2500-3000 m a.s.l., wait for 2 days, and then gradually start to train. At higher altitudes, one should consider a staged ascent (average ascent rate 300 m/day above 2000 m a.s.l.), primarily in order to sleep and feel well, and minimize the risk of mountain sickness. A new classification of altitude levels based on the effects on performance and well-being is proposed and an overview given over the various modalities using hypoxia and altitude for improvement of performance.
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PMID:General introduction to altitude adaptation and mountain sickness. 1866 47

High-dose interleukin-2 (IL-2), given via continuous intravenous (i.v.) infusion, induces lymphokine-activated killer (LAK) cell cytotoxicity against tumor cells. These LAKs exhibit enhanced cytotoxicity against tumor cells in vitro when they are subsequently pulsed with additional IL-2. Famotidine may increase LAK cytotoxicity against neoplastic cells by allowing for greater IL-2 uptake at the IL-2 receptor on lymphocytes. Twenty-three (23) patients received famotidine 20 mg i.v. twice per day and continuous-infusion IL-2 (18 MIU/m(2)/24 hours) for 72 hours, followed by a 24-hour rest, then 1-3 daily-pulse IL-2 doses of 18 MIU/m(2) over 15-30 minutes preceded by famotidine 20 mg i.v. Cycles were repeated every 3 weeks. The most common metastatic sites were lung, lymph node, and subcutaneous/soft tissue. The most common toxicities were fever, rigor, nausea/emesis, hypophosphatemia, hypotension, elevated creatinine, and pulmonary edema. There were no treatment-related deaths. One (1) complete (4%) and 9 partial responses (39%) were seen (43% total response rate; 95% confidence interval: 22%-65%). Median survival for all patients is 13 months. The combination of famotidine and high-dose continuous infusion + pulse IL-2 is active in metastatic melanoma.
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PMID:Activity of continuous infusion + pulse interleukin-2 with famotidine in metastatic melanoma. 1924 44

High altitude sickness is a common name for illnesses that can occur at high altitude, usually above 3000 meters from sea level. The cause is hypoxia but the pathophysiology of the diseases is a complex mixture of multiple factors, involving the human response to hypoxia. The most common symptom is headache, but loss of appetite, nausea and sleep disturbances are also common complaints. With rapid or high ascent there is increased risk of acute mountain sickness, with severe headache that responds poorly to pain medications, nausea, vomiting and extreme fatigue as the most common symptoms. The most severe forms of high-altitude sickness are high altitude cerebral edema and high altitude pulmonary edema. High altitude sickness can be prevented by slow ascent and avoiding overexertion. Medications can also be used to reduce symptoms. In this overview high altitude physiology and acclimatisation are reviewed. The main types of high altitude sickness are described with special emphasis on symptoms and diagnosis, but treatment and prevention are also reviewed.
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PMID:[High altitude sickness - review]. 1949 9

Glyphosate-surfactant (GlySH) is a commonly used herbicide that has been used in attempted suicide. Most reports of GlySH toxicity in patients have followed ingestion of the commercial product "Round-up" (Monsanto Ltd; Melbourne, Victoria, Australia), which consists of a mixture of glyphosate (as a isopropylanine salt) and a surfactant (polyoxyethyleneamine). Ingestion of Round-up is reported to cause significant toxicity including nausea, vomiting, oral and abdominal pain. Renal and hepatic impairment and pulmonary oedema may also occur. Impaired consciousness and encephalopathy have been reported as sequelae but there are limited data on the central nervous system (CNS) effects of Round-up toxicity. We report a 71-year-old male who attempted suicide with GlySH and developed a prolonged but reversible encephalopathy suggestive of acute CNS toxicity.
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PMID:Glyphosate-surfactant herbicide-induced reversible encephalopathy. 2065 31

Postoperative delirium is one of the most spectacular, frightening and misdiagnosed postoperative complications of surgery. We describe the case of a caucasian 77-year-old male patient, who developed a severe postoperative delirium after combined transurethral resection of the prostate and cystolithotripsy. This systemic and unpredictable complication of endoscopic surgery is caused by excessive absorption of electrolyte-free irrigation fluids, leading to brain edema and metabolic encephalopathy. The clinical spectrum ranges from asymptomatic hyponatraemia, to electrocardiographic (ECG) changes, nausea, vomiting, convulsions, coma, pulmonary edema, cardiovascular compromise and death. Because of the heterogeneous clinical presentation diagnosis can be difficult. In a patient who develops alterations of consciousness with evidence of hypervolemia and hyponatremia after endoscopic surgery, transurethral resection syndrome must be considered.
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PMID:Post operative delirium with hyponatriemia after transurethral resection of the prostate: a case of transurethral resection syndrome? 2174 38

Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specific therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fluid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.
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PMID:A systematic review of aluminium phosphide poisoning. 2408 57

The chemotherapeutic streptozotocin is used for induction of diabetes in animal models including non-human primates. Being a cytotoxic nitrosourea compound, it can be associated with adverse events (AEs), mainly nausea and emesis, nephrotoxicity, elevated liver transaminase levels, pulmonary oedema and, most prominently, metabolic acidosis: these can be severe in some cases. The incidence and gravity are to some extent related to the characteristics of the individual animal, diagnostic tools, prompt recognition of symptoms and supportive measures. Careful animal selection, dose adaptation and supportive actions such as renal protective hydration are the main tools in managing AEs, but do not fully eliminate unavoidable and sometimes life-threatening conditions. In our centre we have built experience in a cohort of 78 cynomolgus and rhesus macaques in which six cases manifested severe AEs (8%). This experience has prompted implementation of strategies for early detection and management of adverse effects, together with an animal refinement programme. We present here specific pretreatment regimens, post-infusion laboratory evaluations, and flow charts to assess/treat metabolic acidosis and precipitating factors. Case reports of the six animals with severe AEs are presented to illustrate management of AEs, especially metabolic acidosis, and criteria for early euthanasia where appropriate. We conclude that improved monitoring and validated tools allow for optimal management of adverse effects in an early stage of their manifestation. Reduced morbidity and mortality not only improve individual animal wellbeing but also avoid model-induced confounding that diminishes the translational value of the experimental protocol.
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PMID:Management of adverse side-effects after chemotherapy in macaques as exemplified by streptozotocin: case studies and recommendations. 2257 53

Sudden ascent to high altitudes beyond 2,438 m can cause life-threatening complications such as acute mountain sickness and high altitude cerebral and pulmonary oedema. We present a case of pituitary apoplexy in a young man who ascended to high altitude gradually, after proper acclimatisation. He developed headache, nausea, vomiting and persistent hypotension. Magnetic resonance imaging revealed an enlarged pituitary gland with haemorrhage. His hormonal estimation showed acute adrenal insufficiency due to corticotropin deficiency. The patient responded well to conservative medical management with hormonal replacement therapy. This is most likely the first reported case of high altitude-induced pituitary apoplexy in the literature.
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PMID:High altitude-induced pituitary apoplexy. 2294 Nov 36

The recent outbreak of hantavirus in Yosemite National Park has attracted national attention, with 10 confirmed cases of hantavirus cardiopulmonary syndrome and thousands of more people exposed. This article will review the epidemiology, presentation, workup, and treatment for this rare but potentially lethal illness. The possibility of infection with hantavirus deserves consideration in patients with severe respiratory symptoms with rodent exposure or rural/wilderness travel. Accurate diagnosis requires a high index of suspicion. Hantavirus cardiopulmonary syndrome presents as a vague prodrome of fever, cough, myalgias, chills, and nausea followed by a rapidly worsening respiratory phase. Presumptive diagnosis can be made based on pulmonary interstitial edema on chest radiographs in association with leukocytosis, thrombocytopenia, and hemoconcentration. Suspected cases should be confirmed with a reference laboratory and reported to the appropriate public health authorities. Although treatment is primarily supportive, aggressive fluid administration should be avoided due to the risk of pulmonary edema. The cardiopulmonary phase of the disease can progress rapidly with catastrophic decompensation in as little as a few hours. Patients require rapid intensive care unit admission for monitoring, mechanical ventilation, vasoactive agents, and possibly extracorporeal mechanical ventilation. Emergency physicians should be aware of outbreaks and vigilant for hantavirus exposures, especially during the summer and early fall months.
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PMID:Hantavirus infection in North America: a clinical review. 2368 Mar 31


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