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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Divers breathing compressed air are restricted to 45 m depth because of the narcotic effects of nitrogen and toxic action of oxygen at increased pressures. Substitution of oxygen-helium for compressed air has permitted divers to reach 600 m. However, at depths greater than 160 m, signs and symptoms of the high pressure nervous syndrome (h.p.n.s.) occur, with tremors, myoclonic jerking, nausea, vomiting, fatigue, somnolence, e.e.g. changes, dyspnoea, and poor sleep with nightmares. It has been the objective of this Laboratory to ameliorate the symptoms of pressure-induced h.p.n.s. by the addition of small amounts of 'narcotic' nitrogen to the oxygen-helium mixture to form the Trimix breathing gas. In 1973, comparative experiments with oxygen-helium and the same divers, during compressions in only 33 min to 219.5 m and 305 m, showed such Trimix to be effective with 10% (by volume) nitrogen. Simulated dives, termed ATLANTIS, have been made with Trimix over the last 4 years to depths in excess of 610 m for 11 days, 650 m for 4 days and 686 m for 1 day. The objectives were to determine the effects of either slow or rapid rates of compression, and either 5% or 10% (by volume) nitrogen in Heliox, on the presence of h.p.n.s. or nitrogen narcosis. Measurements were made of intellectual and psychomotor performance, electrophysiological function of the brain and reflexes, lung and cardiovascular function, including arterial gas analysis at rest and work, blood chemistry and psychiatric and psychological status. The results permit the conclusion that divers may be compressed safely to depths as great as 686 m. The technique requires a slow exponential compression over days, with frequent stages lasting 14 h or more, the use of 5-8% (by volume) nitrogen in Heliox and careful selection of the divers.
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PMID:Probing the limits of human deep diving. 614 71

In a series of 250 consecutive open-heart operations, three cases of late cardiac tamponade were noted following the operation. This led the authors to review the literature pertaining to this complication. Ninety-nine cases were collected. The frequency of late tamponade associated with cardiac surgery was 0.62% and was fatal in 16.2% of those cases. The delay before the tamponade appeared varied from 3 days to 3 months (mean 14.5 +/- 7.8 days). The initial clinical picture is insidious and vague, and this constitutes the danger of late cardiac tamponade. The clinical signs are of the respiratory (dyspnea, chest pain), gastrointestinal (anorexia, vomiting) and central nervous (mental confusion, even coma) systems. Pallor with a drop in hematocrit in patients on anticoagulant therapy suggests occult bleeding. A definitive diagnosis depends on catheterization of the right side and on mono- and bidimensional echocardiography. The authors believe that computerized axial tomography represents an interesting noninvasive and reliable examination technique when it can be used during emergency treatment. Pericardial puncture, which is both a diagnostic and therapeutic technique, was useful in one third of the cases; it produced a false-negative result in 12%. The resulting differential diagnoses are pulmonary embolism, myocardial insufficiency and septic shock. Late cardiac tamponade may be produced by one of two mechanisms: hemopericardium due to overdosage of anticoagulants or an exacerbated form of the post-pericardiotomy syndrome. Emergency treatment is always necessary. Pericardiocentesis is a useful diagnostic aid and provides temporary stabilization preoperatively. A wide surgical approach is always indicated. The mortality in untreated patients is 100%. The frequency of immediate relapse or, occasionally, of delayed relapse is estimated to be 11%; relapse may be lethal.
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PMID:[Late tamponade after heart surgery: a dreadful diagnostic pitfall]. 634 35

Contrast media reactions may be classified as anaphylactoid, vasomotor, severe or life threatening, and fatal. Anaphylactoid reactions mimic immunoglobulin E-mediated hypersensitivity in that signs may consist of urticaria, angioedema, wheezing, dyspnea, hypotension, or shock. These reactions occur in 2% to 8% of all contrast media infusions. Vasomotor reactions occur in 5% to 8% of patients and consist of nausea, vomiting, flushing, and warmth. Severe reactions during which there is a concern for life occur about once per 1000 procedures. Fatalities have occurred in from 1:3000 procedures for intravenous cholangiography to between 1:10,000 to 1:100,000 procedures for intravenous urography. The pathogenesis of contrast media reactions is unknown, and various mechanisms may be associated with different clinical features. Radiocontrast media infusions can cause rises in plasma histamine and complement activation by either classic or alternate pathways or nonsequentially, yet adverse reactions may or may not occur. Abnormalities in the complement system or an increased conversion of prekallikrein to kallikrein has been demonstrated in some patients who have had anaphylactoid reactions. It is unknown if these mechanisms can explain the pathogenesis of anaphylactoid contrast media reactions. When patients who have had definite anaphylactoid reactions require a repeat procedure, the incidence of reactions ranges from 35% to 60% for intravascular infusion. Pretreatment with prednisone and diphenhydramine has been demonstrated to reduce this reaction rate to 9% in 465 procedures. Prednisone-diphenhydramine and ephedrine have further reduced the reaction rate to 3.1% in 192 procedures. These results are statistically significant (X2 = 5.4996, p = 0.019). Emergency equipment should be available should a severe reaction occur.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contrast media reactions. 649 Nov 7

Snake bite was diagnosed in 125 dogs and 115 cats over 10 years. Young sporting dogs and young cats were mainly affected. More dogs (48%) were seen in contact with tiger snakes than cats (7%). One hundred and four (84%) dogs and 89 (76%) cats were bitten in the warmer months of the year (October to March). As the incidence rose in September/October, dogs were bitten on days when the temperature was near 20 degrees C or over. The commonest presenting signs were dilated pupils and absences of pupillary light reflex. Dyspnoea, hypothermia, hindleg ataxia and glycosuria were common features in cats. Vomiting, tachypnoea, hyperthermia and complete flaccid paralysis were often seen in dogs. The overall recovery rate after administering antivenene was 90% for cats and 83% for dogs. Death from anaphylaxis as a result of giving antivenene occurred in 3 cats and one dog. Dogs treated soon after being bitten recovered more rapidly. There was no correlation between the bite-to-treatment period and the treatment-to-recovery period for cats.
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PMID:Clinical features therapy and epidemiology of tiger snake bite in dogs and cats. 649 4

A railroad accident in Somerville, Massachusetts, led to spillage of phosphorus trichloride liquid. Attempted clean-up with water led to the liberation of phosphorus trichloride, phosphoric acid, hydrochloric acid, and phosphorus oxides. Seventeen people exposed to this mixture were studied. Patients experienced eye irritation, lacrimination, nausea, vomiting, and dyspnea. Six patients had transient elevation of lactic dehydrogenase. Although all patients had normal chest roentgenographic findings, pulmonary function tests showed statistically significant decreases in vital capacity (p = 0.02), maximal breathing capacity (p = 0.02), forced expiratory volume in one second (p = 0.02), and maximal expiratory flow rate at 25 percent of vital capacity (p = 0.05) in those closest to the accident site. Further, patients exposed for less than one and a half hours had significantly greater maximal expiratory flow rates at 25 percent of vital capacity when compared with patients who had been exposed longer (p = 0.02). In seven patients, repeated pulmonary function tests one month later showed improvement, suggesting strongly that the acute effects may have been due to phosphorus trichloride toxicity.
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PMID:Phosphorus trichloride toxicity. Preliminary report. 650 58

The clinical features and necropsy findings are described for seven trekkers in the Himalayas whose deaths were related to high altitude. The fatal outcome was due to serious pulmonary and cerebral disease. Oedema of the lungs and brain was prominent but so was thrombosis and haemorrhage, features of acute mountain sickness that have received insufficient recognition in the past. Most of the men were middle aged. Some began their trekking soon after flying to high altitude before becoming acclimatised and some remained at high altitude or climbed even higher despite the development of vomiting, breathlessness, and exhaustion. In one case death occurred despite prompt recognition and treatment of symptoms by administration of oxygen and swift evacuation to low altitude.
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PMID:Altitude-related deaths in seven trekkers in the Himalayas. 662 17

A patient at 42 weeks of pregnancy called the emergency department complaining of painful uterine contractions for six hours. She was advised to come to the hospital immediately. An episode of vomiting caused a 60-minute delay in her arrival. Dyspnea, fatigue, and leg cramps developed. In the emergency department she was anxious, alert, and cyanotic. Fetal distress was diagnosed. Within 15 minutes the patient had bradycardic cardiopulmonary arrest. Resuscitation attempts and agonal caesarean section failed. Autopsy revealed massive pulmonary amniotic fluid emboli. Amniotic fluid embolus must be considered in the differential diagnosis of pregnant patients with complaints of shortness of breath and signs of shock with bradycardia.
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PMID:Massive amniotic fluid embolism. 671 33

Four adults, including a pregnant woman, and three children were admitted to hospital following accidental exposure to mercury vapour produced by heating mercury-gold amalgam. Initial symptoms and signs included a paroxysmal cough, dyspnea, chest pain, tachypnea, nausea, vomiting, fever and leukocytosis. Pulmonary function testing performed on the second day after exposure revealed air-flow obstruction and minor restrictive defects in three patients. The diffusing capacity of the lung for carbon monoxide was reduced in two of these patients. The mean initial blood mercury level (+/- one standard deviation) for the seven patients was 30.8 +/- 1.5 micrograms/dl. A computer analysis showed mercury to behave as a two-compartment system, the compartments having half-lives of 2 and 8 days. The four adults received chelation therapy with D-penicillamine, which did not affect the urinary excretion of mercury. The pregnant woman's infant, born 26 days after exposure, had no detectable clinical abnormalities. The levels of mercury in the blood of the mother and infant at birth and 6 days later were comparable, indicating free transfer of the metal across the placenta.
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PMID:Accidental inhalation of mercury vapour: respiratory and toxicologic consequences. 688 61

This case study reports on a 33 year old woman who took oral contraceptives (OCs) for 8 years and who developed gastrointestinal bleeding from esophageal varices. This bleeding was found to be due to the results of a portal vein thrombosis. The woman had taken norgestrel and ethylnylestradiol. Abdominal pain without vomiting and diarrhea, and mild and intermittant dyspnea occurred. At laparoscopy, the volume and the surface of the liver appeared normal; biopsy of the liver was also normal. Celiac and mesenteric angiography demonstrated a portal vein thrombosis. Pulmonary thromboembolism probably occurred first during or immediately after the portal vein thrombosis. Despite immediate anticoagulant therapy, the patient died suddenly some days later. Two factors enhanced the patient's susceptibility to estrogen associated thrombosis: her age of 33 years and that she had taken the pill for over 5 years. OC treatment could have induced thromboembolic disease both in portal and pulmonary circulations in this patient.
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PMID:Portal vein thrombosis and fatal pulmonary thromboembolism associated with oral contraceptive treatment. 697 49

T-2 toxin was given to cats every other day per os to evaluate the suitability of this species as a model for the human disease, alimentary toxic aleukia. The chronic lethal intoxication resulting was characterized by pancytopenia, hemorrhagic diatheses, bone marrow aplasia, diminished hemostasis, severe lymphatic tissue alterations, and histopathologic changes in proliferative tissue. Clinical signs included vomiting, bloody feces, weakness, lassitude, ataxia, dyspnea, dehydration, loss of weight, and pre-terminal anorexia. The clinical course, hematologic picture, and the gross and microscopic tissue changes seen in the experimentally produced disease in cats were similar to alimentary toxic aleukia, a frequently fatal mycotoxin induced disease of man.
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PMID:Experimental alimentary toxic aleukia in cats. 719 59


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