Incidence and clinical importance of perioperative histamine release: randomised study of volume loading and antihistamines after induction of anaesthesia
TL;DR: The histamine-related disturbances under anaesthesia were remarkable for their severity (even with small rises in histamine concentrations), for the prevalence of bradycardia, and for the absence of skin signs.
About: This article is published in The Lancet.The article was published on 1994-04-16 and is currently open access. It has received 136 citations till now. The article focuses on the topics: Antihistamine & Haemaccel.
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University of Antwerp1, University of Manchester2, University of Sydney3, Royal North Shore Hospital4, Gunma University5, Auckland City Hospital6, Sir Charles Gairdner Hospital7, University of Paris8, University of Copenhagen9, Copenhagen University Hospital10, University of Bergen11, Haukeland University Hospital12, Brigham and Women's Hospital13, University of Leeds14, University of Texas Southwestern Medical Center15, Monash University16, University of Western Australia17, Leeds Teaching Hospitals NHS Trust18, Mayo Clinic19
TL;DR: This review summarises recent information on the epidemiology of perioperative hypersensitivity reactions, with specific consideration of differences between geographic areas for the most frequently involved offending agents.
Abstract: Summary Suspected perioperative hypersensitivity reactions are rare but contribute significantly to the morbidity and mortality of surgical procedures. Recent publications have highlighted the differences between countries concerning the respective risk of different drugs, and changes in patterns of causal agents and the emergence of new allergens. This review summarises recent information on the epidemiology of perioperative hypersensitivity reactions, with specific consideration of differences between geographic areas for the most frequently involved offending agents.
85 citations
TL;DR: The role, route of delivery, dose, concentration, and efficacy of the various drugs used in anaphylaxis, including Adrenaline, steroids, antihistamines, fluids, glucagon, aminophylline, and discharge drugs will be discussed in detail.
Abstract: At present there are few controlled clinical therapeutic trials in acute anaphylaxis despite the emergence of evidence based medicine. Moreover, the explosive nature, unpredictable onset, and usually rapid response to treatment that characterise acute anaphylaxis mean that this situation is unlikely to change.' The vast majority of serious anaphylactic reactions occur unexpectedly,2 typically in fit patients. Anaphylaxis is rarely seen or described in critically ill or shocked patients other than in those with asthma.1 Therefore, treatment recommendations have to be based on clinical observation, interpretation of the pathophysiology and, to an extent, animal studies.' However, descriptions of the management of anaphylaxis, for instance those in Hospital Update in 19914 and on angio-oedema in the British Medical Journal in 1992,5 are often then criticised for the treatment recommended.9 A recent expert opinion by Fisher on the treatment of acute anaphylaxis\" was followed by no less than 10 letters in response, many of which contained errors of logic as pointed out by Fisher in replying to them.\" Clearly there is confusion about the correct management of acute anaphylaxis. Much of the controversy is due to misinterpretation of published reports. In this review I reassess the role, route of delivery, dose, concentration, and efficacy of the various drugs used in anaphylaxis. Adrenaline, steroids, antihistamines, fluids, glucagon, aminophylline, and discharge drugs will be discussed in detail. I shall use the term \"anaphylaxis\" to refer to both anaphylactic reactions (IgE mediated immediate type hypersensitivity reactions) and anaphylactoid reactions (non-immunologically triggered), as the clinical expression and final mediators involved are identical.'2 Tables are included giving clear recommendations for first line, second line, and discharge treatment, and allowing rapid evaluation of the drugs involved. Adrenaline
80 citations
TL;DR: Despite over 60 years of clinical practice, the safety and efficacy of gelatin cannot be reliably assessed in at least some settings in which it is currently used.
Abstract: Purpose
Gelatin is frequently used as a volume expander in critical care. Our goal was to investigate its safety.
80 citations
TL;DR: A three-component outcome system including clinician-derived objective, patient-reported subjective end points and qualitative analysis of clinical relevance was developed in the last 10 years for cancer as a complex intervention.
Abstract: BACKGROUND: Despite thousands of papers, the value of quality of life (QoL) in curing disease remains uncertain. Until now, we lacked tools for the diagnosis and specific treatment of diseased QoL. We approached this problem stepwise by theory building, modelling, an exploratory trial and now a definitive randomised controlled trial (RCT) in breast cancer, whose results we report here. METHODS: In all, 200 representative Bavarian primary breast cancer patients were recruited by five hospitals and treated by 146 care professionals. Patients were randomised to either (1) a novel care pathway including diagnosis of ‘diseased’ QoL (any QoL measure below 50 points) using a QoL profile and expert report sent to the patient’s coordinating practitioner, who arranged QoL therapy consisting of up to five standardised treatments for specific QoL defects or (2) standard postoperative care adhering to the German national guideline for breast cancer. The primary end point was the proportion of patients in each group with diseased QoL 6 months after surgery. Patients were blinded to their allocated group. RESULTS: At 0 and 3 months after surgery, diseased QoL was diagnosed in 70% of patients. The QoL pathway reduced rates of diseased QoL to 56% at 6 months, especially in emotion and coping, compared with 71% in controls (P ¼0.048). Relative risk reduction was 21% (95% confidence interval (CI): 0–37), absolute risk reduction 15% (95% CI: 0.3–29), number needed to treat (NNT) ¼7 (95% CI: 3–37). When QoL therapy finished after successful treatment, diseased QoL often returned again, indicating good responsiveness of the QoL pathway. CONCLUSION: A three-component outcome system including clinician-derived objective, patient-reported subjective end points and qualitative analysis of clinical relevance was developed in the last 10 years for cancer as a complex intervention. A separate QoL pathway was implemented for the diagnosis and treatment of diseased QoL and its effectiveness tested in a community-based, pragmatic, definitive RCT. While the pathway was active, it was effective with an NNT of 7.
79 citations
Cites background from "Incidence and clinical importance o..."
...…years) and staff problems (number of participants and changes), has, however, successfully been completed twice before: for induction of anaesthesia and perioperative cardio-respiratory complications (Lorenz et al, 1994) and for sepsis following surgery for colorectal cancer (Bauhofer et al, 2007)....
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TL;DR: Plasma tryptase levels were not significantly elevated in confirmed anaphylactoid reactions, so they can be used to distinguish chemical from immunologic reactions.
Abstract: Background: Anaphylaxis, mediated by immunoglobulin E, may be clinically indistinguishable but is mechanistically different than chemically mediated anaphylactoid reactions induced by drugs such as morphine, curare, and vancomycin. A test to distinguish anaphylactic from anaphylactoid reactions would clarify therapeutic and medicolegal issues. Tryptase levels identify anaphylactic reactions but have not been evaluated in vivo during anaphylactoid reactions. A prospective, randomized, double-blinded, placebo-controlled trial of antihistamine chemoprophylaxis for rapid vancomycin infusion was performed, and plasma tryptase was measured using a new immunoassay. Histamine release was established by measurement of plasma histamine and the ability of prophylactic H 1 and H 2 antagonists to prevent common histamine-associated side effects. Tryptase levels were compared with histamine levels and clinical symptoms. Methods: Before elective arthroplasty, 40 patients received vancomycin infusion (1 g over 10 min) and pretreatment with either antihistamines (1 mg/kg diphenhydramine and 4 mg/kg cimetidine) or placebo. Changes in tryptase (at peak histamine and 10 min after vancomycin infusion), histamine levels, and histamine-mediated symptoms were assessed using Fisher's exact test, the Student's t test, or the paired t test, as appropriate. Logistic regression models were used to quantify the association of clinical symptoms with antihistamine treatment and serum levels. Results: Plasma tryptase levels were unchanged (99% CI, -0.5 to 1.6) independent of increased histamine levels, antihistamine pretreatment, clinical symptoms, or all of these. Histamine levels >1 ng/ml were significantly associated with hypotension, moderate-to-severe rash, and stopped infusion. Antihistamine pretreatment significantly decreased the incidence and severity of the reactions. Conclusion: Plasma tryptase levels were not significantly elevated in confirmed anaphylactoid reactions, so they can be used to distinguish chemical from immunologic reactions.
77 citations
References
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Journal Article•
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2,147 citations
TL;DR: 80 reports of randomised clinical trials in four leading general medical journals were reviewed and the reporting of the methodology of randomisation was inadequate, and the handling of comparisons of baseline characteristics was inadequate.
473 citations
TL;DR: The electrocardiographic changes consistent with ischemia during the 4 day perioperative period were documented and characterized in 100 patients with or at risk for coronary artery disease undergoing noncardiac surgery and postoperative ischemic episodes were the most severe.
321 citations
TL;DR: Pancuronium is suggested to be the least likely currently available agent to provoke a major anaphylactoid reaction and Predisposing factors in patients sensitive to muscle relaxants were: female sex, previous allergy and atopy.
Abstract: Sixty one patients who had suffered intra-operative anaphylactoid reactions were studied. Intradermal testing identified the causative agent in 84% of cases and, in 75% of these, muscle relaxants were responsible. Predisposing factors in patients sensitive to muscle relaxants were: female sex, previous allergy and atopy. The incidence of previous exposure was considerably higher than that reported in the literature. Pancuronium is suggested to be the least likely currently available agent to provoke a major anaphylactoid reaction.
130 citations
TL;DR: The effects of increasing concentrations of three opioids were studied on the release of preformed and de novo synthesized chemical mediators from human peripheral blood basophils and mast cells isolated from skin tissues or lung parenchyma.
Abstract: Opioids differ in their capacity to cause release of histamine. The effects of increasing concentrations of three opioids (morphine, buprenorphine, and fentanyl) were studied on the release of preformed (histamine and tryptase) and de novo synthesized (prostaglandin D2 [PGD2] and peptide-leukotriene C4 [LTC4]) chemical mediators from human peripheral blood basophils and mast cells isolated from skin tissues or lung parenchyma. Basophils released < 5% of their histamine content and did not synthesize significant amounts of LTC4 when incubated with any of the opioids. Mast cells showed markedly different responses to the three opioids. Morphine (10(-5)-3 x 10(-4) M), in a concentration-dependent manner, induced histamine and tryptase release from skin but not from lung mast cells, up to a maximum of 18.2 +/- 1.9% and 13.0 +/- 4.1 micrograms/10(7) cells, respectively. Morphine did not induce de novo synthesis of PGD2 from skin mast cells. Buprenorphine (10(-6)-10(-4) M), in a concentration-dependent manner, caused histamine and tryptase release from lung but not from skin mast cells, to a maximum of 47.6 +/- 7.2% and 35.1 +/- 13.6 micrograms/10(7) cells, respectively. Buprenorphine also induced de novo synthesis of PGD2 and LTC4 from lung mast cells. Fentanyl (10(-5)-10(-3) M) did not induce histamine and tryptase release or the de novo synthesis of PGD2 or LTC4 from any mast cells. Histamine release caused by buprenorphine from lung mast cells was slow (t1/2 = 11.2 +/- 3.6 min) compared with that induced by morphine from skin mast cells (t1/2 < 1 min, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
113 citations