Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1986-1988, adverse anaphylactoid reactions (AR) were observed in animals in Czechoslovakia after the administration of oil adjuvant-containing vaccines or other lipoid drugs. Treated animals showed signs resembling the classic anaphylactic reaction, i.e. restlessness, salivation, pruritus, oedema and cyanosis of udder and vulva, and eyelid oedema, developing within a few minutes. The reactions were not elicited by the antigen alone, but by the oil adjuvant. The aim of our experiments was to identify substances eliciting the reaction in susceptible animals and to investigate possible induction mechanisms. The emulsifier Tween 80 has been demonstrated to be an AR inducing component of vaccines and drugs (Tab. I and III). Weak or moderate reactions were observed in 33% of animals treated with 5% Tween and 66% of those treated with 10% Tween showed strong reactions. On the other hand, no reactions were elicited by treatment with several paraffin oils of different quality (Tab. I) nor with an oil-in-water emulsion containing Montanid as an emulsifier (Tab. II). The role of the vegetative nervous system in the rise of AR has been confirmed. AR were suppressed in animals pretreated with parasympatholytic atropine and enhanced in a part of those pretreated with parasympathomimetic pilocarpine (Tab. III). The percentage of animals affected and the intensity of AR were also lower in animals pretreated with complement inhibitor epsilon-aminocapronic acid (Tab. IV). A major role of complement activation is suggested in the discussion of possible mechanisms of AR induction. It is possible to draw a conclusion on the basis of the results presented here and of the analysis of individual cases that a certain degree of animal susceptibility, depending on the phase of reproductive cycle, metabolism level and neurovegetative balance is necessary besides the administration of an AR inducer (Tween 80 in our case). Hence it seems that the adverse anaphylactoid reactions results from interactions of the two factors, i.e. administration of an AR inducer to susceptible animals.
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PMID:[Causes of anaphylactoid reactions in cattle after administration of lipoid preparations]. 148 39

A 32-year-old female patient was operated on for a residual colonic stricture occurring after hemicolectomy. A right internal jugular central venous catheter was inserted during the anaesthetic for postoperative parenteral feeding. The anaesthetic combined both general and epidural anaesthesia, the latter being continued for postoperative analgesia (10 ml.h-1 of 0.125% bupivacaine). Two days later, the patient complained of sudden chest pain, with restlessness, tachycardia, cyanosis, resulting in ventricular tachycardia and cardiac arrest. When admitted to the surgical intensive care unit, the patient was in deep coma and had nonsustained ventricular tachycardia, a left haemopneumothorax and a pneumopericardium. The patient died before a definitive diagnosis was made. Postmortem examination revealed an ulcerated anterior pillar of the tricuspid valve, as well as a perforation of the right ventricle and a communication between the pericardium and the left pleural cavity. The diagnosis and treatment of this rare life-threatening complication may be very difficult. It prevention consists in using short catheters for internal jugular venous access, and checking the tip's position radiologically by opacifying the catheter.
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PMID:[Cardiac tamponade and central venous catheterization]. 150 94

A case of double aortic arch is reported. The male patient, 11-month-old, had breathed with a constant stridor since his birth and had frequent attacks of respiratory tract infection and dyspnea. The child was admitted because of restlessness, fever, stridor and cough. Dyspnea with cyanosis appeared later, and required intubation and mechanical ventilation. After then, three attempts to extubate the infant were made, but failed. A double aortic arch was suspected by bronchogram, esophagogram, and confirmed by cardiac catheterization. Through a left thoracotomy, the smaller left arch and the ligmentem arteriosum were divided to relieve the obstruction of trachea from the compression of the vascular ring. Postoperative convalescence was normal. Symptoms of double aortic arch vary with the degree of obstruction of the trachea and esophagus, ranging from mild to life-threatening respiratory obstruction and apnea. Inspiratory stridor, dyspnea, and wheezing, which are accentuated with feeding, crying, or respiratory infections, are characteristic clinical findings. The diagnosis is established by aid of an esophagography. Left thoracotomy, with division of the smaller aortic arch, is the only satisfactory treatment.
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PMID:[Double aortic arch: report of one case]. 263 8

The case of a 3-week-old male infant is described. After receiving an iatrogenic overdose of metoclopramide (1.0 mg/kg every six hours) throughout a 36-hour period for the treatment of suspected gastroesophageal reflux, he became cyanotic, lethargic, and irritable, he fed poorly, and he had diarrhea and respiratory distress. Methemoglobinemia (20.5%) and reduced oxyhemoglobin saturation (79%) were identified. The patient had an excellent clinical response following a single IV dose of methylene blue. Subsequently, methemoglobin reductase activity was normal and there was no measurable hemoglobin M. The diagnosis of methemoglobinemia should be considered in any infant receiving large doses of metoclopramide who has clinical findings of cyanosis, ashen color, or a history of lethargy and/or motor restlessness.
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PMID:Metoclopramide-induced methemoglobinemia. 340 65

Hypoxic and hypercapneic arousal responses from quiet sleep were tested in 56 infants with apnea of infancy (one or more episodes of cyanosis, limpness, and apnea requiring vigorous stimulation or resuscitation with no treatable cause; age 6.8 +/- 1.1 [SEM] months). Responses were compared with those of nine control infants ranging from 1 to 25 months of age. To assess hypercapneic arousal, the inspired PCO2 was rapidly increased during quiet sleep to 60 mm Hg or until arousal (restlessness, agitation, eye opening) occurred. All control infants and those with apnea of infancy aroused to hypercapnea, but control infants aroused at a lower inspired PCO2 (inspired PCO2 40.1 +/- 2.6 mm Hg) than those with apnea of infancy (inspired PCO2 46.9 +/- 1.5 mm Hg, P less than .05). To assess hypoxic arousal, the inspired PO2 was rapidly decreased during quiet sleep to 80 mm Hg or until arousal occurred. All control infants aroused to hypoxia (inspired PO2 78.3 +/- 2.1 mm Hg). However, only 38% of those with apnea of infancy aroused (inspired PO2 78.1 +/- 0.8 mm Hg), indicating an abnormality in recognition of hypoxia, or central brainstem response to hypoxia. During the 10.4 +/- 1.2 months of follow-up, there was a high incidence of subsequent apneas (greater than 20 seconds) during sleep at home in 50 apneic infants. Infants with abnormal hypoxic arousal responses had more severe subsequent apneas than those with normal hypoxic arousal responses (P less than .05).
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PMID:Hypoxic and hypercapneic arousal responses and prediction of subsequent apnea in apnea of infancy. 399 Dec 71

Studies of the arterial blood gas tensions and pH in 21 children during 24 acute attacks of asthma showed that all were hypoxic on admission to hospital, and in 10 there was evidence of carbon dioxide retention. Cyanosis, invariably present when the So(2) was below 85%, and restlessness in patients breathing air were the most reliable indices of the severity of hypoxia. There were no reliable clinical guides to the Pco(2) level. Conventional oxygen therapy in tents (25-40%) did not always relieve hypoxia, and in three cases the administration of oxygen at a concentration of 40% or over failed to produce a normal arterial oxygen tension. Uncontrolled oxygen therapy may aggravate respiratory acidosis, and three of our patients developed carbon dioxide narcosis while breathing oxygen. The necessity for blood gas measurements in the management of severe acute asthma in childhood is emphasized.
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PMID:Arterial blood gas tensions and pH in acute asthma in childhood. 566 2

Croup syndromes are common in children, most frequently being infectious in origin. Children present with a slow progression of inspiratory and expiratory stridor and a croupy, "barking seal" cough. Children are variably febrile and with progression of disease, exhaustion, agitation, cyanosis and air hunger may develop. The evaluation of the patient must focus on the degree of respiratory distress and associated findings. Epiglottitis and foreign body aspiration must be excluded. Management is primarily dependent upon administration of humidified air. Children with moderate to severe croup benefit from racemic epinephrine and steroids. Admission is indicated in children with stridor at rest, evidence of exhaustion, toxicity or respiratory distress. Active airway intervention is rarely required but may be life saving if obstruction develops.
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PMID:Croup: pathogenesis and management. 638 67

Experimental studies to this point have not identified a selective neonatal pulmonary vasodilator. They have indicated that the neonatal pulmonary circulation is a complex, active vascular bed that has a number of endogenous vasodilatory mechanisms which oppose vasoconstriction under normal circumstances. It seems likely that a better understanding of how those mechanisms become deranged in various disease states will be required before we can substantially improve our drug therapy in pulmonary hypertensive infants. The data we have outlined above indicate that firm recommendations for drugs and their doses cannot be made. Nonetheless, several principles of therapy can be outlined. Because of the marginal benefits, which have resulted from current drug therapy [9, 24, 34, 79, 84, 100, 107], it seems clear that, at the moment, the most prudent initial course in neonates with pulmonary vasospasm should be nonpharmacologic: restoration of normal blood gases, use of high concentrations of inspired oxygen with hyperventilation to pH 7.6 if cyanosis persists [22, 79], avoidance of agitation and hypothermia [22], and correction of any metabolic derangements [92]. Decreased cardiac output should be identified and treated with blood volume expanders and/or cardiotonic agents as necessary. Finally, if physiologic efforts to lower pulmonary vascular resistance fail, drug therapy sometimes is helpful in effecting salvage. Treated infants should be carefully monitored, not only for signs of improved oxygenation, but also for changes in right-to-left ductal shunting and cardiac output. If a given agent does not produce beneficial effects at a range of doses by 60 min, it is unlikely that prolonged therapy will result in late improvement. In such circumstances, a change in drug therapy is probably indicated. Finally, it would seem wise to use multiple agents with extreme cautions, being careful to pair a direct vasodilator (e.g., nitroprusside, tolazoline, or prostacyclin) with a cardiotonic agent (e.g., isoproterenol or dopamine), or simultaneously administered volume expanders as the individual clinical situation dictates. Further animal experimentation will undoubtedly identify new and promising agents and provide an increasing understanding of the cellular physiology of the newborn pulmonary circulation. However, only careful clinical and experimental studies into the cause(s) of the vasoconstriction in newborns will allow the development of a truly rational approach to specific therapy in the human species.
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PMID:Neonatal 'pulmonary vasodilator' drugs. Current status. 642 57

We studied diaphragmatic muscle function during inspiratory flow resistive (IFR) loaded breathing in unanesthetized sheep. We measured the change in transdiaphragmatic pressure (dPdi) and arterial blood gas tensions and recorded diaphragmatic electromyogram (EMG) from electrodes implanted on the muscle. We found that, with IFR loads less than 150 cmH2O X l-1 X s, dPdi and the integrated EMG increased, reached a plateau, and were maintained at high levels. The centroid frequency (fc) of the EMG power spectrum did not consistently change. With IFR loads greater than 150 cmH2O X l-1 X s, O2 was administered to prevent hypoxia, cyanosis, and agitation. With these loads, dPdi increased severalfold above base line, reached a plateau, and then started to decrease. Arterial PCO2 increased sharply at the time when dPdi decreased. The integrated EMG (iEMG) and fc started to decrease gradually 10-20 min before dPdi started to decrease. We conclude that 1) the diaphragm is capable of generating large pressures for prolonged periods with no evidence of fatigue; 2) with very high IFR loads, mechanical failure of the diaphragm can occur in the unanesthetized awake sheep; 3) diaphragmatic fatigue is associated with acute hypercapnia and therefore failure of the entire respiratory pump; and 4) a decrease in iEMG and a concommitant shift in the power spectrum density towards lower frequencies precede the mechanical failure of the diaphragm.
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PMID:Diaphragmatic fatigue in unanesthetized adult sheep. 646 79

Tracheomalacia is a rare congenital malformation of the tracheobronchial cartilages in which the supporting cartilaginous rings permit expiratory collapse of the airway. The condition is usually mild and self-limited. There is a severe variant, however, that is life-threatening and warrants separate categorization. Four children with severe primary tracheomalacia were treated recently. The clinical symptoms, diagnostic findings, and eventual treatment of these patients were highly distinctive and almost identical in all 4, permitting us to make the following observations: (1) primary severe tracheomalacia must be suspected in infants with unexplained respiratory distress manifested by stridor and cyanosis; (2) symptoms are not present at birth but appear insidiously after the first weeks of life, are markedly aggravated by respiratory tract infections, and are made worse by agitation; (3) bronchoscopy is essential for definitive diagnosis and should be employed early in the diagnostic process; (4) tracheostomy is probably essential in most instances; and (5) resolution, although spontaneous, does not occur until after 2 years of age.
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PMID:Primary tracheomalacia. 684 90


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