Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tricyclic antidepressant overdose is the most common cause of death from prescription drugs. Clinical presentation of overdose from the tricyclic agents includes cardiac arrhythmias, hypotension, seizures, coma and anticholinergic signs such as hyperthermia, flushing and intestinal ileus. The highly toxic/lethal level (greater than 1,000 ng per mL) is manifested on electrocardiograms as prolongation of the QRS interval to 100 milliseconds or more. Treatment includes establishment of an airway, proper oxygenation and ventilation, fluid replacement at maintenance levels, cardiac monitoring, gastric lavage and charcoal administration, alkalinization to a blood pH of 7.5 with intravenous sodium bicarbonate, supportive therapy and continued cardiac monitoring after clinical recovery.
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PMID:Managing tricyclic antidepressant overdose. 162 27

The major use of N-acetylcysteine in clinical toxicology is in the treatment of acetaminophen (paracetamol) overdosage. The hepatorenal toxicity of acetaminophen is mediated by a reactive metabolite normally detoxified by reduced glutathione. If glutathione is depleted, covalent binding to macromolecules and/or oxidation of thiol enzymes can lead to cell death. Oral or intravenous N-acetylcysteine or oral D,L-methionine mitigates acetaminophen-induced hepatorenal damage if given within 10 hours, but becomes less effective thereafter. In vivo, N-acetylcysteine forms L-cysteine, cystine, L-methionine, glutathione, and mixed disulfides; L-methionine also forms cysteine, thus giving rise to glutathione and other products. Oral therapy with N-acetylcysteine or methionine for acetaminophen poisoning is contraindicated in the presence of coma or vomiting, or if activated charcoal has been given by mouth. Nausea, vomiting, and diarrhea may also occur as a result of oral N-acetylcysteine administration. Anaphylactoid reactions including angioedema, bronchospasm, flushing, hypotension, nausea/vomiting, rash, tachycardia, and respiratory distress may occur 15-60 minutes into N-acetylcysteine infusion (20 hours intravenous regimen) in up to 10% of patients. Following accidental intravenous overdosage, the adverse reactions of N-acetylcysteine are similar but more severe; fatalities have occurred. A reduction in the loading dose of N-acetylcysteine may reduce the risk of adverse reactions while maintaining efficacy. Administration of N-acetylcysteine for a longer period might provide enhanced protection for patients in whom acetaminophen absorption or elimination is delayed. N-acetylcysteine may also have a role in the treatment of toxicity from carbon tetrachloride, chloroform, 1,2-dichloropropane, and other compounds. The possible use of N-acetylcysteine and other agents in the prevention of the neuropsychiatric sequelae of acute carbon monoxide poisoning is an important area for future research.
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PMID:Use of N-acetylcysteine in clinical toxicology. 192 4

Ethanol sensitivity is a syndrome of flushing, tachycardia, weakness, fatigue, and other dysphoric symptoms in response to relatively small doses of ethanol. We describe a case of extreme ethanol sensitivity presenting with coma and review the pathophysiology of the syndrome.
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PMID:Ethanol sensitivity. 192 88

Animal experimental studies conducted at the turn of the century resulted in the use of magnesium sulphate as an anticonvulsant in humans. In U.S. clinics, parenteral administration of magnesium sulphate became a routine procedure in the treatment of eclampsia and pre-eclampsia. This treatment has proved very effective in treating convulsions in pregnancy provided an adequate dosage was given amounting to up to 60 g daily. Mother and infant mortality were largely eliminated. Numerous clinical studies showed a negligible side effect rate. Side effects in the foetus: These are due to penetration of magnesium into the foetal blood circulation. Reports on an inhibition of cardiac rate fluctuation and changes in calcium levels have been contradictory, and hence not generally accepted. It is claimed that the parathormone level may drop slightly. Isolated reports on foetal magnesium intoxications associated with depression of breathing, slackness and hyporeflexia often prompt the conclusion that this disease pattern had been due to immaturity and asphyxia. Generally, foetal magnesium blood levels do not correlate well with signs of magnesium intoxication. Urine excretion is greatly slowed down in foetal immaturity. Side effects in the mother: Short-term relaxing action on the uterus has been described frequently. High dosages have been successfully used in arresting labour if there is a tendency to premature birth. Increase in uterine blood flow was seen after administration of magnesium sulphate in animal experiments. Magnesium is said to reduce blood coagulation by influencing fibrinolysis and thrombocyte resistance. However, a somewhat enhanced loss of blood during birth is said to be more likely due to relaxation of the uterus than to a disturbance of blood coagulation. Rapid intravenous injection causes short-term flushing, nausea and vomiting. Short-acting drops in blood pressure are possible. The cardiac output is said to increase at the conventional dosage level whereas the peripheral resistance drops due to vasodilation. Increases and decreases in heart rate have been reported, but in most cases no changes were seen. Changes in ventricular action time occur with toxic doses only, which can lead to cardiac arrest in the diastole. Other toxic signs are hyporeflexia, depressed breathing and CNS depressions which may result in coma. Hyporeflexia always occurs before the other toxic signs appear, so that it can be used as a clinical control criterion. Calcium gluconate, given via the IV route, is a good and rapid-acting antidote.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Use of magnesium sulfate as an anticonvulsant in severe pregnancy toxemia and eclampsia]. 655 75

We describe a patient treated with trazodone, isocarboxazid, and methylphenidate hydrochloride who developed confusion, agitation, poor concentration, rigidity, myoclonus, involuntary movements, orthostatic hypotension, and hyperreflexia. CK was normal, and the syndrome resolved spontaneously over 12 hours. The serotonin syndrome occurs following the use of serotomimetic agents (serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, tryptophan, 3,4-methylenedioxy-methamphetamine, dextromethorphan, meperidine, S-adenosylmethionine) alone or in combination with monoamine oxidase inhibitors. It is characterized by various combinations of myoclonus, rigidity, hyperreflexia, shivering, confusion, agitation, restlessness, coma, autonomic instability, low-grade fever, nausea, diarrhea, diaphoresis, flushing, and rarely, rhabdomyolysis and death.
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PMID:Serotonin syndrome. 785 15

We describe severe sertraline intoxication in a child after accidental ingestion. Sertraline is a new antidepressant that has potent and selective inhibition of neuronal serotonin reuptake. Drug company-sponsored research has suggested little toxicity for this compound. Our patient exhibited prolonged tachycardia, hypertension, hallucinations, coma, hyperthermia, tremors of all extremities, and skin flushing. Clinicians should consider the possibility of serotonin syndrome among patients with similar clinical features and a recent history of sertraline or other serotonergic agent ingestion.
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PMID:Sertraline intoxication in a child. 819 16

The feasibility of intratracheal pulmonary ventilation (ITPV) was tested in five ventilated moribund neonatal and pediatric patients with uncontrollable hypercapnia: a 2-year-old child, a 52-day-old infant, and three premature infants (29, 29, and 26 weeks gestation; 1300 g, 1100 g and 890 g birth weight, respectively). ITPV was applied for 9.5, 8, 25, 58.5, and 47.5 hr, respectively. An intratracheal catheter (Cook Critical Care, Inc., Bloomington, IN) with a reversed continuous flow of gas at its tip (away from the lungs) allowed flushing of CO2 from the proximal dead space. Marked reductions in Paco2, ranging from 37% to 71% and improvement in pH were achieved within 4-6 hr of applying ITPV. During ITPV, the mean lowest Paco2 was significantly less than the pre-ITPV Paco2 (p < 0.0017), and the mean best pH was significantly higher than the pre-ITPV pH (p < 0.015). In four patients, despite significant reductions in Paco2, there was no substantial improvement in their baseline condition (shock and severe metabolic acidosis or coma) and they were switched back to conventional ventilation. This led to worsening hypercapnia to pre-ITPV values. These four patients subsequently died. It is possible that these patients were already too ill to derive significant benefit from the technique. One premature infant survived, was successfully weaned to conventional ventilation and was eventually discharged home. ITPV can alleviate uncontrollable hypercapnia in ventilated neonatal and pediatric patients.
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PMID:Intratracheal pulmonary ventilation in premature infants and children with intractable hypercapnia. 946 6

Digestive neuro-endocrine tumours have a broad and initially misleading clinical spectrum. Tumours from the duodenopancreatic area should be distinguished from digestive carcinoid tumours. In the first group, insulinomas, gastrinomas, and non-functioning tumours are the most frequent. Insulinoma is responsible for hypoglycaemic symptoms (coma, confusion, seizure, psychiatric disorders) associated with adrenergic response (sweat, tachycardia, palpitations). Gastrinoma is responsible for the Zollinger-Ellison syndrome, which associates peptic ulcers in the oesophagus, stomach, and duodenum without Helicobacter pylori infection, and chronic volumogenic diarrhoea. Non-functioning tumours are recognised fortuitously or at a late stage, when large tumour mass contrasts with often unaltered general condition. Carcinoid tumours are mainly located in the appendix, the rectum, and the small bowel. In the 2 first conditions, the diagnosis is most often made on a resection specimen after uneventful appendectomy or polypectomy; in the latter, the carcinoid syndrome is frequent, combining cutaneous flushing, motor diarrhoea, tricuspid valve insufficiency and bronchospasm.
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PMID:[Clinical spectrum of digestive neuroendocrine tumors]. 1192 15

In response to a question on how to avoid the rare, inadvertent intravascular or ip injection of hypertonic saline solution during therapeutic abortion, 3 consultants replied. According to Reid and Frigoletto, to avoid intravascular or ip infusion, place a small indwelling polyethylene catheter in the amniotic sac rather than a metal needle. This virtually precludes the possibility of inadvertent iv injection. When and if necessary, correct catheter placement may be confirmed by the use of fluoroscopy and amniography prior to the injection of hypertonic saline solution. The chemical imbalances associated with this accident are those encountered in severe hypernatremia with resultant brain edema and hemorrhagic softening. Bizarre paresthesia, pyrexia, altered consciousness, and, eventually, convulsions preceded the fatal cases. Peritoneal dialysis may be life saving in the event of ip injection. Naturiuretics, appropriate parenteral fluid administration, and possibly exchange transfusion might be indicated for intravascular accidents. In Goodlin's hospital there have been no cases of acute hypernatremia in the last 500 therapeutic abortions done with hypertonic saline solution. This is believed to be related to 2 changes in technique: 1) not losing the amniotic space by removing only as much amniotic fluid as can easily be obtained and 2) using a simple gravity infusion technique for the instillation of the hypertonic saline solution. During infusion it is essential that the patient be alert, for the first symptoms of intravascular injection are a slight pain, burning, or a feeling of warmth in the pelvis. If these minor symptoms are ignored and the procedure is continued, a sensation of flushing occurs throughout the body with tingling in the scalp and ringing in the ears followed finally by seizures, apnea, or coma or both. Late symptoms are those of hemolytic anemia and renal failure. From experience, serum sodium levels during these events are as high as 185 mEq/1. Along with occurrence of acute hypernatremia the contents of the amniotic cavity are sometimes extruded extraovularly through the fallopian tube into the peritoneal cavity when labor begins. Cases with serum sodium levels of 170 mEq/1 some 6-7 hours after saline instillation were observed, but by contrast these patients' only symptoms were extreme thirst and peritoneal discomfort (Lancet 1: 305, 1968). The treatment of hypernatremia is to force fluids either by mouth or iv. Since most commercial 5% dextrose in water solutions are actually 4.5% (regulations permit a 10% error), such hypotonic fluids are useful for treating hypernatremia.
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PMID:Hypernatremia from intravascular saline infusion during therapeutic abortion. 1230 84

Mechanical ventilation (MV) during exacerbation of asthma or chronic obstructive pulmonary disease (COPD) is unequivocally needed when apnoea, cardiorespiratory arrest, coma, hypoxia or treatment failure is present. The need is less clear when the patient can respond, has intact airway reflexes and spontaneous respiration. In this situation, acidosis is an important factor in the decision to institute MV. This study aimed to provide a clinical means of identifying patients with acute respiratory acidosis (ARA) in a setting where blood gas analysis is unavailable. We undertook a prospective, observational study of consecutive patients who presented to two emergency departments with severe and life-threatening exacerbation of asthma or COPD. Each underwent clinical assessment, treatment and blood gas analysis. The outcome measure was ARA or mixed ARA and metabolic acidosis. A total of 127 episodes in patients aged 15-90 years (65.3% males and 34.7% females) were included in the study. Of these, 62.2% had asthma and 37.8% had COPD; 71.7% had life-threatening and 28.3% had severe attacks. Overall, the adjusted odds ratio (and 95% confidence intervals) for predictors of ARA were 7.09 (1.79-28.06) for drowsiness, 4.11 (1.31-12.88) for flushing, 3.34 (1.01-11.02) for having COPD and 2.86 (1.01-8.07) for intercostal retractions. In conclusion, with drowsiness, the likelihood of ARA is about seven times higher. The presence of flushing, COPD and intercostal retractions also increase the risk of ARA.
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PMID:Clinical predictors of acute respiratory acidosis during exacerbation of asthma and chronic obstructive pulmonary disease. 1239 18


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