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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apart from sufficient experience on the part of the examining physician and adequate technical apparatus, proper premedication can facilitate the procedures for both patient and physician considerably. The paper reports on experience gained in 500 laparoscopies carried out under conditions which were deviated slightly from those hitherto recommended in the literature. The analgesic employed was Tilidine (in Germany: Valoron), and Diazepam was used as a sedative; both of these substances were given intravenously, the vein was kept open for the entire course of the examination. The Tilidine dose was normally 50-100 mg, but under exceptional circumstances as much as 150 mg. Tilidine showed good analgesic effectiveness and tolerance; no case or nausea or vomiting and no sign of respiratory depression of effects on smooth muscle were observed under the conditions stated. The fact that Tilidine is not subject to the restrictions imposed by the German narcotics law is also seen as an advantage. The Diazepam dose was 5-30 mg. Apart from its sedative effect Diazepam also diminishes the tonus of skeletal muscle (important in laparoscopy) and has a relatively long time of elimination (20-48 h). In addition to these two substances, 10-20 ccm of 1% Lidocaine solution with Epinephrine additive was given as a local anaesthetic. The investigators' experience with the above premedication procedure was found to be convincingly positive.
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PMID:[Premedication with valoron (Tilidin) in internal laparoscopy]. 13 78

Patients receiving exogenous corticosteroids may develop iatrogenic adrenal insufficiency, with resultant nausea, emesis, and abdominal distension if perioperative "stress steroid" dosages are inadequate. To investigate these gastrointestinal disturbances, motility measurements were obtained using perfused catheters in 10 dogs before steroid treatment (control), during administration of high-dose corticosteroids, and daily during 5 days of abrupt withdrawal. Withdrawal was characterized by a significant disruption in normal antral, duodenal, and jejunal motility with a prolongation of the migrating motor complex (MMC) and phases I and II, but not III (I = quiescence, II = irregular activity, and III = regular activity). Retrograde giant contractions (RGCs), giant migrating contractions (GMCs), and/or "intestinal fibrillation" were also observed during the first two withdrawal days. Adrenal weights and morphology did not change. We conclude: (1) high-dose corticosteroids can induce profound adrenal suppression in dogs without morphologic changes within 3 weeks; (2) high-dose steroid administration enhances gastrointestinal motility; and (3) acute withdrawal causes disappearance or shortening of MMC and the development of RGCs and GMCs with associated emesis.
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PMID:Alterations in gastrointestinal motility during postoperative acute corticosteroid withdrawal. 192 86

We compared gastric myoelectrical activity and endogenous neuroendocrine responses in subjects with and without motion sickness elicited by illusory self-motion or vection. Rotating a drum with black and white vertical stripes around seated stationary subjects (n = 22) produced vection. Gastric myoelectrical activity was recorded with cutaneous electrodes. Thirteen subjects developed gastric dysrhythmias [4- to 9-cycles/min (cpm) signals] and motion sickness during vection, whereas nine subjects maintained normal 3-cpm gastric rhythms and remained symptom free. Base-line plasma cortisol and beta-endorphin levels were significantly greater (P less than 0.01) in the subjects who would develop gastric dysrhythmias and nausea compared with the subjects who would not develop motion sickness. Norepinephrine levels increased in the nauseated group immediately after vection ceased (354.6 +/- 41.1 pg/ml) compared with the symptom-free subjects (223.1 +/- 22.8 pg/ml, P less than 0.05). Epinephrine increased significantly (P less than 0.05) after vection only in the nauseated subjects, whereas dopamine levels were not altered by vection in either group. We conclude that 1) anticipatory increases in plasma cortisol and beta-endorphin occurred in subjects who would develop nausea and gastric tachyarrhythmias during vection; 2) endogenous epinephrine and norepinephrine were increased in subjects who had vection-induced nausea and gastric dysrhythmias; and 3) vection stimulates brain-gut interactions, resulting in gastric tachyarrhythmias and complex neuroendocrine responses in subjects with motion sickness.
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PMID:Neuroendocrine and gastric myoelectrical responses to illusory self-motion in humans. 213 78

The diagnosis of adrenal haemorrhage complicating heparin therapy is often delayed, despite computed tomography (CT). Moreover, its pathogenesis is not clear. Adrenal haemorrhages are often seen in cases where there is no unduly excessive anticoagulation, and can be accompanied by a paradoxical thrombosis of the central adrenal vein. Symptoms usually occur within the first 8 to 12 days after starting heparin. The difficulty in establishing the diagnosis stems from the fact that symptoms are rather nonspecific: abdominal pain and backache, nausea, vomiting, lethargy, weakness, hypotension, hyperpyrexia. To confirm the diagnosis, both hormonal proof of adrenal failure and anatomic evidence of haemorrhage must be found. Early CT scans may show the haemorrhage. Several possible causes have been put forward to account for these adrenal haemorrhages. The degree of anticoagulation did not seem to be a prerequisite, 30 to 50% of patients showing no evidence of other bleeding or coagulation tests outside the therapeutic range. Capillary fragility of old age might be a factor. Stress would seem to be an important factor predisposing to adrenal haemorrhage. Many authors consider the paradoxical central vein thrombosis as a result of the haemorrhage rather than its cause, whereas other conclude the opposite. Unfortunately, to date coagulation studies are often incomplete; platelet counts were missing in most reports published before 1985. Since that date, a heparin induced thrombosis-thrombocytopaenia syndrome (HITTS), in which thrombosis may occur in any vascular bed, has been recognized with increasing frequency. Nine cases of adrenal haemorrhage associated with HITTS have been reported. It seems highly likely that a proportion of cases of heparin-related adrenal destruction are due to HITTS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hematoma of the adrenal glands and heparin]. 269 74

Seven male volunteers were given apomorphine (14-20 micrograms/kg) subcutaneously on a total of ten occasions. Nausea was experienced on six occasions and on four occasions there was no effect. Venous samples were taken before injection, at peak nausea and 20 min later for assay of factor VIII coagulant activity (FVIIIC), von Willebrand factor antigen (vWFAg), the ristocetin cofactor (FVIIIRiCof), euglobulin clot lysis time (ECLT), fibrinopeptide A (FPA), FPA generation time, activated partial thromboplastin time (APTT), vasopressin (aVP) and adrenaline. During nausea plasma aVP concentrations rose from median values of 0.4 pg/ml (at time 0) to 76 pg/ml at peak nausea and fell to 32 pg/ml 20 min later. Adrenaline rose from 0.36 to 0.91 nmol/l (P less than 0.05) before falling to 0.55 nmol/l. During nausea, FVIIIC rose from 100% to 143% (P less than 0.05) and to 214% (P less than 0.05) 20 min later. FVIIIRiCof and vWFAg showed similar changes. Plasminogen activator activity (10(6)/ECLT2) rose from 23 units at time 0 to 592 units during nausea and 1135 units (P less than 0.05) after 20 min. The APTT fell from 49 s to 44 s during the study, plasma FPA levels and the FPA generation time both remained unchanged. On the four occasions nausea was not experienced, there were no changes in vasopressin and catecholamine concentrations nor in haemostatic function. During the study, plasma aVP concentrations rose to levels previously shown to influence haemostatic function. This provides further support for the view that aVP has a secondary role as a mediator of acute changes in haemostasis, and during nausea contributes with adrenaline to an abrupt change in factor VIII and fibrinolytic activator activity.
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PMID:Vasopressin and catecholamine secretion during apomorphine-induced nausea mediate acute changes in haemostatic function in man. 376 10

Intestinal graft-versus-host disease (GVHD) causes anorexia, vomiting, abdominal pain, and diarrhea. We investigated oral beclomethasone dipropionate (BDP), a potent, topically active corticosteroid, as therapy for this disease. Forty-two allogeneic marrow-graft recipients with biopsy-proven intestinal graft-versus-host disease of mild-to-moderate severity received BDP (8 mg daily) for up to 28 days. Weekly symptom scores, oral intake, and surveillance throat and stool cultures were compared with baseline values. Adrenal testing was performed serially in patients not receiving concurrent prednisone. Improvement was seen in appetite (P < 0.001), oral intake (P < 0.001), nausea (P = 0.013), and diarrhea (P = 0.02) over the course of therapy, and an overall beneficial response was observed in 72% of 40 evaluable patients. Surveillance cultures of throat and stool showed no increase in bacterial or fungal colonization over time. The adrenal axis became suppressed in 11 of 20 evaluable patients (55%) but suppression was not a prerequisite for clinical response, as 6 of 9 patients who retained normal adrenal function improved clinically. We conclude that oral BDP is a safe and effective treatment for mild-to-moderate intestinal graft-versus-host disease. Systemic absorption probably occurs, but adrenal suppression is not a prerequisite for clinical efficacy, suggesting that the biological effect is primarily topical. BDP should be further investigated as a topical therapy for intestinal GVHD.
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PMID:Oral beclomethasone dipropionate for treatment of human intestinal graft-versus-host disease. 852 16

The features of the symptoms, laboratory tests and pathological characteristics of adrenal cortical and medullary hyperplasia were studied. In 6 cases of hypercatecholaminenia, plasma norepinephrine (NE), epinephrine (E), catecholamine (CA) and 24-h urinary vanillylmandelic acid (VMA), 17-hydroxycorticosteroid (OHCS) and 17-ketosteroid (KS) were determined. Adrenal glands were examined by CT scan and 131I-MIBG imaging. Pathological examination was performed after operation. The results showed that in 6 cases of hypercatecholaminenia (3 men and 3 women) aged from 34-50 years, the clinical features were just like "pheochromocytoma", for example, episodic headache, perspiration, palpitation, pallor, apprehension, nausea, tremor, anxiety and so on. Plasma levels of CA, NE and E were elevated in all 6 cases. 24-h urinary samples obtained at the onset revealed elevated VMA in 1 case. 24-h urinary cortisol was obviously elevated in all 6 cases. 24-h urinary 17-OHCS, 17-KS was normal. B-type ultrasound, CT, MRI and 131I-MIBG revealed 9 lateral adrenal gland diffuse or nodular enlargement in 6 cases. Pathologic examination showed adrenal cortical and medullary hyperplasia. Clinically, adrenal cortical and medullary hyperplasia resembled "pheochromocytoma". The most significant feature of this disease was both elevated plasma CA and 24-h urinary cortisol obviously. Pathologic examination showed adrenal cortex nodular hyperplasia and medullar diffuse or limit hyperplasia. Whether it is an independent disease or symptoms of the other disease has not final conclusion up till now.
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PMID:Adrenal cortical and medullar hyperplasia--a retrospective analysis of 6 cases. 1267 82

This was a great save. The crew could easily have missed the presentation of anaphylaxis and let the window for treatment with epinephrine slip away. This patient was in anaphylactic shock. There were no signs that supported a traumatic injury, and that, combined with diaphoresis, urticaria and tachycardic central pulse, contributed to the suspicion of anaphylaxis. Anaphylaxis is classified as distributive shock. This type of shock is caused by profound systemic vasodilation, and the heart is unable to increase output enough to maintain blood pressure. Other causes of distributive shock include sepsis and spinal cord injury. It is rare to have both hypotension and wheezing in such cases. In an anaphylactic reaction, an allergen, such as a food protein, medication, insect venom or latex, is introduced into the body. The mast cells of the immune system have a protein on their surface called IgE antibodies (Immunoglobulin E). The mast cells are filled with histamines [table: see text] and leukotrienes, which are chemical mediators. These are released when the allergen reacts with the IgE antibodies. When these mediators are released, they cause smooth-muscle constriction in the respiratory and gastrointestinal tracts, resulting in wheezing, stridor, nausea, vomiting and diarrhea. They also cause vascular dilation, leading to edema and urticaria. Most patients will present with either profound vascular effect (shock) or wheezing; this is a rather rare presentation of a patient having both. The medication best suited to counteract the effects of these medicators is epinephrine. Epinephrine is an alpha- and beta-agonist, acting to constrict the vasculature and dilate the smooth muscles in the bronchial tree. Antihistamines can alleviate symptoms of anaphylaxis, but should only be used in addition to epinephrine, not as a substitute. In life-threatening reactions, epinephrine must be given quickly and in a form that the body can distribute. Use of the subcutaneous route with a solution mixed at 1:1,000 dilution is appropriate in most patients, but if the patient is in profound shock and not perfusing the skin (pale, cold, clammy skin), then a more diluted concentration must be given i.v. at a slow rate (1 cc every minute of the 1:1,000 dilution) until the patient recovers. If i.v. access is delayed or not available, give the 1:1,000 dilution intramuscularly, in the tongue or down the endotracheal tube. Refer to your local protocols for dosage, but the usual dose of epinephrine is 0.3-0.5 mg, or 0.01 mg/kg in a child. There are more than 40 million people in the U.S. with allergic histories that place them at risk for developing anaphylaxis. Each year over 5,000 deaths are attributed to anaphylaxis. The risk of death from anaphylaxis increases with a more rapid onset of signs and symptoms. Up to 25% of patients will experience a biphasic reaction. This means there is a recurrence of symptoms several hours after the initial reaction, and it is prudent to observe patients for a period of time following their initial treatment.
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PMID:Bugged. 1277 12

Stapedotomy for otosclerosis presents particular anaesthesiology demands as the surgeon has to assess functional results during the operation, work with some bleeding, be ensured the collaboration of the patient, and limit the occurrence of intra- and post-operative symptoms (dizziness, nausea, vomiting and pain). Remifentanyl, a micro-opioid selective agonist characterised by short latency and duration, has been used for about 2 years at the Otolaryngological Unit of the "Federico II" University of Naples for patients with otosclerosis undergoing stapedotomy. Aim of the study was, therefore, to assess: efficacy and tolerability of Remifentanyl in combination with a local anaesthetic in surgical procedures for otosclerosis; intra- and post-operative reduction in patient symptoms of dizziness, nausea, vomiting and pain; reduction of intra-operative bleeding; degree of patient collaboration and optimisation of anaesthesiological and vital parameters monitored during surgery. The study was carried out on 92 patients with otosclerosis, (17 M, 75 F), median age 41 years (range 25-56), undergoing stapedotomy. Patients were randomly assigned to one of two groups, which were homogeneous as far as concerns age, sex and pre-operative hearing: i. Group A (50 patients), received Remifentanyl infusion in combination with canal injection for local anaesthesia with Mepivacaine 2% and Adrenalin 1/100,000; ii. Group B (42 patients), received only local anaesthetic by infiltration of the external canal ear. Remifentanyl led to an improvement over the local anaesthetic technique previously used, with a clear decrease in intra- and post-operative neurovegetative symptoms such as dizziness, nausea, vomiting and pain, as well as reduced bleeding.
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PMID:Use of Remifentanil for sedo-analgesia in stapedotomy: personal experience. 1595 79

Addison's disease is a rare disorder in patients with end-stage renal disease (ESRD). In patients, the diagnosis of Addison's disease is difficult in clinical practice because most of the clinical findings of this disease are similar to those of the renal failure. We present a 51-year-old male patient, who underwent hemodialysis therapy for 8 years, diagnosed with Addison's disease after having myalgia, skin hyperpigmentation, weight loss, sweating, and nausea for the past few weeks. The physical examination was completely normal except for muscle weakness, hyperpigmentation on labial mucosa and skin in a patient. The laboratory tests revealed anemia and hypoglycemia. Serum cortisol, adrenocorticotropic hormone (ACTH) levels, and ACTH stimulation test results were consistent with Addison's disease. Adrenal computerized tomography revealed bilateral atrophic glands. Additionally, it was found that elevated serum thyroid stimulating hormone levels and antithyroid peroxidase antibody titer were positive. Our purpose is to emphasize that physicians should be alert to the potential for additional different conditions particularly in terms of adrenal failure in patients with ESRD.
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PMID:Misdiagnosis of Addison's disease in a patient with end-stage renal disease. 2121 12


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