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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This case presented the scenario of a patient who had severe bronchospasm from an unknown etiology. Further, she had difficulty speaking and denied any past medical history, which made a diagnosis more difficult. Prehospital providers were challenged with determining the differential diagnosis for bronchospasm and hypoxemia. Was the patient experiencing an anaphylactic reaction, acute asthmatic attack or something else? The key here, once again, is conducting a thorough assessment and patient history. Remember, all that wheezes is not asthma; therefore, providers in this case had to determine if the patient was suffering something such as anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart failure (CHF). Typically, anaphylaxis and asthma affect ventilation, not oxygenation, so until the late stages of anaphylaxis or asthma, the patient will have difficulty moving air, but will be oxygenating OK. We understand that many respiratory conditions can cause wheezing, but CHF? Yes: As left ventricular function diminishes and leads to increased pulmonary pressure, serum begins to leak out of the pulmonary vessels and into the interstitial space. As the interstitial pressure increases, it causes narrowing of the bronchioles, and air traveling through the narrowed bronchioles causes the wheezing sound. Fluid may also be leaking out of the pulmonary capillaries and occupying space in the alveolar sacs. When the interstitial pressure is high and the bronchioles continue to narrow, providers may initially hear only the wheezing and not the crackles from the smaller airways. In these conditions, oxygen is not exchanged adequately into the blood, and the patient becomes hypoxemic. Good assessment and patient history will guide the EMS provider to the cause of bronchospasm. For example, does the patient have a history of asthma? If yes, asthma is likely to be the cause. Does the patient have any rash, hives or swelling? If yes, anaphylaxis is likely the cause. Is the patient elderly, and does he/she show pedal edema, JVD, hypoxemia and/or distended neck veins? If yes, CHF may be the cause. [table: see text] There are questions regarding the use of bronchodilators in patients suffering CHF. If a CHF patient is wheezing (bronchospasm), then a beta-2 selective breathing treatment may be appropriate, along with nitrates and diuretics. Oxygenation is the critical problem in CHF, and hypoxemia will continue to worsen cardiac function. Remember, both bronchoconstriction and alveolar sacs filling with fluid will impair oxygenation of the RBCs and ultimately the vital organs. Focused prehospital management of CHF is aggressive in restoring oxygenation. For example, many agencies are now using oxygen, nitrates, ACE inhibitors and CPAP. By better understanding the pathophysiology of respiratory emergencies and their differential diagnosis, we will improve patient outcomes.
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PMID:Breathless. 1196 14

Cis-atracurium is a stereoisomer of atracurium, about five times more potent than the racemate. Whereas cis-atracurium is routinely used in adults, its effects on children are still poorly defined. We compared equipotent doses of atracurium and cis-atracurium in children aged between 2 and 12 years regarding the quality of neuromuscular blockade, the intubation conditions and the occurrence of side-effects. After approval by the ethics committee and with informed parental consent, 84 children (ASA I or ASA II) were randomly allocated to receive either 0.5 mg/kg atracurium (group A, n = 42) or 0.1 mg/kg cis-atracurium (group C, n = 42). In both groups anaesthesia was induced with 15 micrograms/kg alfentanil and 5-7 mg/kg thiopentone. We assessed the intubation conditions according to the Krieg Scale. Anaesthesia was maintained with a nitrous oxide/oxygen mixture of 2:1 and isoflurane in an endexpiratory concentration of approximately 0.6 Vol.%. Neuromuscular blockade was controlled acceleromyographically in response to supramaximal stimulation of the ulnar nerve. We measured the onset time (T1 = 5%), duration of effect (T1 = 25%), recovery index (T1 = 25%-75%) and the recovery time at a train-of-four-ratio (T4/T1) of 0.7. These parameters did not show any significant differences between group A and group C: onset time: 3.1 +/- 1.5 min (group A) versus 3.4 +/- 1.1 min (group C), duration of effect: 34.1 +/- 5.5 min (group A) versus 34.1 +/- 6.5 min (group C), recovery index: 9.3 +/- 3.3 min (group A) versus 9.6 +/- 2.5 min (group C), recovery time at a TOF-ratio of 0.7:49.3 +/- 8.4 min (group A) versus 52.3 +/- 6.6 min (group C). In group A, the intubation conditions were "excellent" or "good" in 98% of the patients, whereas in group C the figure was only 69%. Regarding side-effects, we found significantly more frequent urticaria in group A (6 of the 42 patients) (p < or = 0.05) than in group C, in which no patient showed urticaria. Flush and tachycardia occurred much less frequently and there were no significant differences in the two groups: two patients in group A and only one in group C. The authors conclude that atracurium and cis-atracurium lead to comparable neuromuscular effects in children aged between 2 and 12 years. Only the intubation conditions were better after atracurium, but atracurium was followed by urticaria more often than cis-atracurium.
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PMID:[Cis-atracurium--an equivalent substitution for atracurium in pediatric anesthesia?]. 1223 66

Clinically, one must be able to differentiate between an allergic reaction and an adverse reaction. Clinical manifestations of allergic reactions range from urticaria and rash to bronchoconstriction, laryngeal edema, hematologic disorders, and other serious reactions. Many drugs administered in the perioperative setting can cause allergic reactions. Antibiotics such as penicillins, beta-lactam antibiotics, and sulfonamides are the most common class of drugs that produce allergic reactions. A detailed allergy history is important when deciding if a patient can receive a drug that may cross-react (eg, a cephalosporin in a patient with a penicillin allergy). Vancomycin can cause a reaction that ranges from erythema and pruritus to clinically significant hypotension. Proper dilution and rate of administration are essential in minimizing the histamine from vancomycin that is thought to produce this reaction. "Sulfa allergy" describes an allergy to sulfonamide antibiotics; a patient with a "sulfa allergy" is not allergic to drugs containing sulfur, sulfites, or sulfates. Although true allergic reactions to opioids are rare, naturally occurring compounds like morphine and codeine can cause allergic reactions. After stopping the offending drug, mild allergic reactions can be managed with diphenhydramine, with or without a steroid. Significant allergic reactions require more aggressive management with oxygen, intravenous fluids, epinephrine, and histamine blockers.
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PMID:Allergic reactions to drugs: implications for perioperative care. 1247 5

Both experimental and clinical studies have shown that oxygen-derived free radicals rise in the plasma after thermal injury and participate in the pathogenesis of tissue damage. Hence, various antioxidant molecules have been used in treatment of burn injury both experimentally and clinically. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, is known to have potent antioxidant property. The purpose of the present study was to investigate the effects of CAPE on oxidative stress in plasma of burned rats. Experiment was designed in three groups of rats with 20% full-thickness burn: (a) sham burn (n = 7); (b) burn only (n = 22); (c) burn + treatment with CAPE (n = 22). Plasma levels of malondialdehyde (MDA), nitric oxide (NO) and the activities of xanthine oxidase (XO), and superoxide dismutase (SOD) were used as both bio-indicators of oxidant status and determinant of antioxidant effect of CAPE. They were assessed by biochemical methods at 1st, 3rd, 7th, and 14th post-burn days. In conclusion, CAPE was shown to possess antioxidant activity by saving SOD activity, preventing XO activity and decreasing the levels of MDA, and NO. Our study showed that CAPE may be beneficial in burn injury.
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PMID:The effect of CAPE on lipid peroxidation and nitric oxide levels in the plasma of rats following thermal injury. 1501 18

The skin is exposed to endogenous and environmental pro-oxidant agents, leading to the harmful generation of reactive oxygen species (ROS). The resulting oxidative stress damages proteins, lipids, and DNA. An imbalance between ROS and antioxidants can lead to an elevated oxidative stress level. Some evidence indicates that allergic and inflammatory skin diseases like atopic dermatitis, urticaria and psoriasis are mediated by oxidative stress. For example, monocytes from patients with atopic dermatitis are primed to generate ROS in response to zymosan, a Toll-like receptor 2 (TLR2) ligand, suggesting that Staphylococcus aureus may damage lesional skin of the disease by production of ROS. Mast cells generate mainly intracellular ROS following the aggregation of FceRI; these ROS may act as secondary messengers in the induction of several biological responses. The present review summarizes the involvement of ROS in the pathogenesis of allergic and inflammatory skin diseases.
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PMID:Oxidative stress in allergic and inflammatory skin diseases. 1612 29

Adverse drug reactions with an immunological basis (ADRIB) may involve activation of other concomitant, non-specific mechanisms, amplifying the specific response and contributing to the severity and duration. One concomitant mechanism could be the generation of reactive oxygen species (ROS) and/or their detoxification by anti-oxidants, including anti-oxidant enzymes. We analysed the activity of the anti-oxidant enzymes Cu/Zn-superoxide dismutase (SOD), catalase (CAT) and cellular glutathione peroxidase (GPX), as well as certain markers of oxidative damage (thiobarbituric acid reactive substances (TBARS) and carbonyl content) in peripheral blood mononuclear cells from patients with non-immediate ADRIB using spectrophotometric methods and the anti-oxidant enzymes expression by quantitative real-time reverse transcription-polymerase chain reaction. SOD activity and expression were increased in all types of non-immediate reactions (urticaria, maculopapular exanthema and toxic epidermal necrolysis). Regarding oxidative damage, TBARS were increased in urticaria and maculopapular exanthema, and carbonyl groups in all types of reactions. Our observations indicate that oxidative damage occurs in non-immediate reactions. Carbonyl stress and the inadequacy of the anti-oxidant defences are probable causes.
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PMID:Anti-oxidant enzyme activities and expression and oxidative damage in patients with non-immediate reactions to drugs. 1687 48

Although oxidative damage is known to be involved in inflammatory-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory diseases. Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives, has antioxidant, anti-inflammatory and antibacterial properties. For that reason, we aimed to investigate the efficiency of CAPE administration in preventing oxidative damage in pyelonephritis (PYN) caused by Escherichia coli. In this study, 35 Wistar rats were grouped as follows: control, PYN 24 h, PYN 48 h, PYN 72 h, CAPE 24 h, CAPE 48 h and CAPE 72 h. E. coli (1 x 10(9) c.f.u.) were inoculated into the rats in both PYN and CAPE groups via urethral catheterization. Ten microM/kg-body weight CAPE was injected to the rats in all CAPE groups 24 h before E. coli infection, and injections were repeated at 24-h intervals. Rats were sacrificed 24 h, 48 h and 72 h after infection in both PYN and CAPE groups. Malondialdehyde (MDA) and nitric oxide (NO) levels were significantly increased in kidneys of PYN groups. The activities of the antioxidant enzymes, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and xanthine oxidase (XO) were also elevated by E. coli. However, CAPE administration reduced MDA and NO levels, as well as XO activity, although it increased SOD and GSH-Px activities. Histopathological examination showed that CAPE reduced the inflammation grade induced by E. coli. In conclusion, CAPE administrations decrease the oxidative damage occurring in PYN and therefore could be used for medical management of bacterial nephropathy.
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PMID:Caffeic acid phenethyl ester suppresses oxidative stress in Escherichia coli-induced pyelonephritis in rats. 1705 18

We report 4 patients who had facial color changes to a blue-green-gray color and decreased oxygen saturation as measured by pulse oximetry. Patient 1 received an intravenous (IV) methylene blue solution during a urologic procedure, and the remaining three patients were administered subcutaneous indigo carmine (patient 2) or Patent Blue (Patients 3 and 4) for axillary lymph node mapping. All patients had above normal methemoglobin levels. Two (Patients 2 and 3) had hypotension, and one (Patient 3) required IV ephedrine to restore hemodynamic stability. Patient 4 had a hypersensitivity reaction characterized by systemic urticaria and blue-colored subintegumentary edema due to the subcutaneous administration.
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PMID:Blue dyes, blue people: the systemic effects of blue dyes when administered via different routes. 1757 32

Hymenoptera are the large group of insects which includes honey-bees, bumble-bees, paper wasps, hornets, ants. Female hymenoptera possess specialized stinging apparatus with which they inject their venom into prey's or intruder's body. It could be life-threatening for people sensitive to the venom. The hymenoptera venom consists of mixture of biologically active substances, eg. enzymes (phospholipases, hialuronidase), peptides (melittin, apamin, mastoparans, bombolitins) and low-molecular-weight compounds (biogenic amines, acetylcholine, carbohydrates, lipids, free amino acids). Several types of reactions are possible to develop after stinging by hymenopteran insects: (1) non-allergic local reaction (pain, small oedema, redness at the site of the sting); allergic reactions: (2) large local reaction (extensive local swelling, exceeding 10 cm, persisting longer than 24 hours) and (3) anaphylaxis (generalized urticaria, bronchospasm, hypotension, cardiovascular collapse, loss of consciousness); (4) systemic toxic reaction (oedema, vomits, diarrhoea, headache, hypotension, seizures, altered mental status); (5) unusual reactions (cardiac ischaemia, encephalomyelitis et al.). Therapeutic management after stings includes removing of the stinger (bee stings), local remedies (ice-packs, topical steroids) and prevention and treatment of an anaphylactic shock (epinephrine, general steroids, beta-mimetics, fluid resuscitation, oxygen therapy). In the present review types of reaction after hymenoptera stings were described with special interest of anaphylactic and toxic reactions as well as therapeutic management after stings.
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PMID:[Hymenoptera stings]. 1772 87

Anaphylaxis is an IgE mediated severe allergic reaction causing release of vasoactive substances from mast cells and basophils after re-exposure to an antigen. Signs and symptoms include flushing, urticaria, hypotension, tachycardia, bronchospasm, cardio-respiratory arrest etc. It can occur at induction of anaesthesia when multiple drugs are being administered, but prompt diagnosis with correct management is the key to a successful outcome. This case report describes a patient who developed severe bronchospasm with difficulty in inflating the lungs and dropping oxygen saturations, alongwith hypotension, tachycardia and widespread flushing, at induction of anaesthesia for elective breast surgery. She was promptly managed and her hypotension was corrected, but the bronchospasm was more resistant to treatment. The patient also developed ST segment elevation, which was successfully managed with intravenous glyceryltrinitrate. The bronchospasm responded slowly to salbutamol and aminophylline. The patient underwent surgery and was discharged home on the third postoperative day.
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PMID:Severe anaphylactic reaction at induction of anaesthesia. 1807 42


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