Anaphylactoid reactions after cisatracurium administration in six patients.

IMPLICATIONS: We report six cases of anaphylactoid reaction after the administration of the muscle relaxant cisatracurium. They include two first-time documented anaphylactoid reactions after a precurarising dose. These incidents challenge existing views of a substantially reduced anaphylactoid potential of cisatracurium relative to other muscle relaxants.     

Histamine2 receptor blocker in the treatment of protamine related anaphylactoid reactions: two case reports

Two case reports are described of acute anaphylactoid reactions following the administration of protamine to reverse the anticoagulation effect of heparin in patients undergoing coronary artery bypass graft surgery. The administration of cimetidine seemed to reverse the anaphylactoid reaction after conventional treatment with epinephrine, H1 receptor blocker, and steroids had failed. We recommend that H2 receptor blockade be included with other drugs in the treatment of anaphylactoid reactions following protamine, and possibly after anaphylactoid reactions associated with other substances.     

Anaphylactoid Reaction to Etomidate: Report of a Case

We report an anaphylactoid reaction to etomidate twice in a 60-year-old male with coronary artery disease and peripheral vascular disease. Following the first anaphylactoid reaction, the patient developed myocardial infarction. In addition, the patient’s blood was moderately positive for latex antibodies, which made the differential diagnosis difficult. We concluded that the patient had anaphylactoid reaction to etomidate due to the temporal relationship to induction with the drug. The patient did not manifest similar reaction to other induction drugs used for other surgeries. The patient recovered from both incidents of anaphylactoid reaction to etomidate following intravenous administration of epinephrine and fluids.     

Sideeffects of colloids (author's transl)]

A prospective controlled trial during 1975 and 1976 has revealed that none of the colloids in clinical use (plasma protein solution, gelatine, hydroxyethylstarch and dextran) is free from the risk of anaphylactoid reactions. Even though the incidence of anaphylactoid reactions is low (0.03%), lethal outcome might be encountered. Between the colloids differences exist as far as manifestation (skin, circulatory and respiratory system) and degree of severity (I--IV) of anaphylactoid reactions are concerned. Since the underlying pathomechanisms have not been elucidated yet, true prophylactic measures are unknown. Therefore, it is mandatory to control the patient very carefully at the beginning of infusion; early symptoms of anaphylactoid reactions should trigger immediate therapeutic measures. Recent findings showed that the anaphylactoid reactions to dextran might be elicited by immune complexes. A new model was developed to investigate the chances of specific prophylactic procedures.     

Role of cytokines in anaphylactoid reaction with marked eosinophilia in a hemodialysis patient

Hemodialysis is rarely terminated by events associated with anticoagulants. A 69-year-old woman on hemodialysis due to chronic renal failure (CRF) developed an anaphylactoid reaction with hypereosinophilia. On the basis of clinical and laboratory findings, we concluded that the causes of this anaphylactoid reaction were low-molecular-weight heparin and heparin. Our patient also showed high levels of soluble interleukin-2 receptor (sIL-2R) and eosinophil cationic protein (ECP), which decreased after the cessation of hemo-dialysis. To date, there has been no report of high levels of cytokines induced by hemodialysis-associated anaphylactoid reaction. In this report, we discuss the mechanism underlying drug-induced anaphylactoid reaction, particularly that involving eosinophilia and cytokines.     

Anaphylactoid reactions to Dextran 40 and 70: reports to the United States Food and Drug Administration, 1969 to 2004

BACKGROUND: Clinical dextrans, such as Dextran 40 and Dextran 70, are associated with anaphylactoid reactions caused by dextran-reactive immunoglobulin G antibodies. When infused immediately before clinical dextrans, dextran 1 significantly reduces the incidence of severe anaphylactoid reactions. The objective of the study was to describe the frequency and characteristics of reports submitted to the United States Food and Drug Administration (FDA) for anaphylaxis or anaphylactoid events after clinical dextran administration. METHODS: We searched the FDA's Adverse Event Reporting System for reports associated with a clinical dextran and describing anaphylaxis/anaphylactoid reactions. Our case definition for a probable anaphylaxis/anaphylactoid event required signs or symptoms from at least two body systems, with at least one sign or symptom being hypotension, vasodilation, or respiratory difficulty, and onset within 60 minutes. Other reports were considered possible cases if the reporter specifically described the reaction as anaphylaxis or an anaphylactoid reaction. Premier RxMarket Advisor provided estimates of total US hospitalizations with clinical dextran or dextran 1 administration from 2000 to 2004, based on discharge billing data from a sample of US hospitals. The IMS National Sales Perspective provided estimates of total doses of dextrans sold in the United States from 1999 to 2004, based on volumes of dextrans sold in a sample of retail and nonretail outlets. RESULTS: The FDA received 366 clinical dextran adverse event reports from 1969 to 2004, of which 90 (24.6%) were anaphylaxis/anaphylactoid events. The ratio of hospitalizations where clinical dextran was administered to hospitalizations where dextran 1 was administered was 28.4:1. The expected ratio would be 1:1 if all clinical dextran patients had received dextran 1 pretreatment. The ratio of clinical dextran doses sold to dextran 1 doses sold in the United States was 38.6:1. CONCLUSIONS: A high proportion of adverse event reports for clinical dextrans described anaphylaxis or anaphylactoid reactions. Hospital discharge and product sales data suggest that dextran 1 has not been used consistently before clinical dextran administration in recent years. To reduce the risk of anaphylactoid reactions, physicians should consider routine administration of dextran 1 before the infusion of a clinical dextran.     

Anaphylactoid Reaction to Dextran—A Report of 133 Cases

From 1968 to 1975, the Swedish Adverse Drug Reaction Committee received 113 reports on anaphylactoid reaction to dextran 70, and 20 reports on the same reaction to dextran 40. For 1975, this would equal a reported incidence of anaphylactoid reaction to dextran 70 of 1:2,500. The median age of patients reacting to dextran 70 was 63 years. Median age increased with increasing severity of the anaphylactoid reaction: from 48 years in patients who died. Symptoms were noticed within 10 min of the start of the infusion, or before 100 ml had been infused in 96 patients (85%) with an anaphylactoid reaction to dextran 70. There was a tendency for severe reactions to be observed earlier than milder ones. Symptoms also tended to be observed earlier in conscious than in unconscious patients. Reactions reported to have occurred in unconscious patients tended to be more severe than those in conscious patients. Patients with anaphylactoid reaction to dextran 40 did not differ from those with reactions to dextran 70 with regard to age, severity of the reaction or time before onset of symptoms. There was one death in this group.     

Extracorporal therapy with AN69 membranes in combination with ACE inhibition causing severe anaphylactoid reactions: still a current problem?

The negatively charged membrane AN69 is known to evoke anaphylactoid reactions both without and with concomitant ACE inhibition. Underlying reasons are mainly the induction of bradykinin release due to the negatively charged membrane and the reduced degradation of bradykinin due to ACE inhibition. This complication has been reported repeatedly, but anaphylactoid reactions still occur in clinical practice. We recently had to treat two patients who suffered anaphylactoid reactions during extracorporal therapy with an AN69 membrane and simultaneous ACE inhibition. The first incident occurred in a patient on hemodialysis, the second was in a patient on continuous venovenous hemofiltration. An anaphylactoid reaction induced by an AN69 membrane during continuous, extracorporal treatment in combination with ACE inhibition has not been reported so far. Our report intends to serve as a reminder that the potentially lethal combination of AN69 membranes with ACE inhibitor treatment should be avoided.     

A case of latex anaphylactoid reaction starting with respiratory symptoms

We report a case of latex anaphylactoid reaction in a 39-year-old man with aortitis. He was scheduled to undergo stent-graft implantation. When the operation progressed into his abdomen, respiratory symptoms, wheezing and high airway pressure, occurred. However, he did not show any dermal symptoms. Thirty-five minutes after the start of respiratory symptoms, his face suddenly showed flush, and intravenous epinephrine worked successfully against anaphylactoid reactions. There are anaphylactoid reactions which occurred with respiratory symptoms, and we should be aware of these cases.     

Treatment of systemic reactions to contrast media

Serious systemic reactions caused by currently used ionic and nonionic contrast material are the anaphylactoid (allergic-like) reaction and the vagal reaction. Each likely has more than one etiology, and certain patients are at higher risk for developing such a reaction. The urologist and radiologist must be able to differentiate between the clinical manifestations of the anaphylactoid (asthma-like) reaction and the vagal (bradycardia and hypotension) reaction. Specific treatment for the anaphylactoid reaction is low-dose epinephrine; specific treatment for the vagal reaction is intravenous fluid and high-dose atropine.     

Ethylene Oxide (ETO) as a Major Cause of Anaphylactoid Reactions in Dialysis (A review)

Ethylene oxide (ETO), an alkylating compound of high chemical reactivity, is widely used for gas sterilization, but recently serious ETO side reactions have been recognized. With chronic ETO exposure, increased spontaneous abortion, sister chromatid exchange, and leukemia are observed. After medical use of ETO outside nephrology, contact dermatitis, cardiopulmonary shock (during cardiopulmonary surgery), allergic local reactions to ETO sterilized lenses, and anaphylactoid reactions to ETO sterilized catheters have been described. In numerous dialysis patients widespread hypersensitivity to ETO has been documented by skin prick test and ETO radioallergosorbent test (RAST). Furthermore an anaphylactoid "first-use reaction" was described in dialyzed patients, most of whom were using hollow-fiber dialyzers. After long discussions whether complement activation versus hypersensitivity is the cause of such acute anaphylactoid reactions, more recent studies using either ETO RAST or basophil degranulation tests implicate ETO hypersensitivity as their major cause. The high prevalence of sensitization to ETO and the frequency, unpredictability, and potential danger of anaphylactoid reactions to ETO lead to the conclusion that ETO sterilization of dialyzers should be discontinued, since alternative modalities of sterilization are currently available.     

Cost identification analysis for succinylcholine

The cost of a dose of succinylcholine from society's perspective equals the acquisition cost of the drug plus the cost of its adverse outcomes. We hypothesized that although the acquisition cost of succinylcholine is minimal, the true cost would be much larger. We reviewed the medical literature to identify the total cost of a dose of succinylcholine when administered for nonemergency purposes according to manufacturers' guidelines (i.e., to adults only). We found that 88% of the cost per dose of succinylcholine was for the chance of dying or sustaining permanent brain injury from anaphylactic or anaphylactoid reactions to succinylcholine. Consequently, the estimated cost per dose of succinylcholine was sensitive to the incidence of anaphylactic or anaphylactoid reactions to succinylcholine, the risk of severe injury from anaphylactic or anaphylactoid reactions, and the financial value of unforeseen instant death or permanent brain injury. The range for the cost per dose of succinylcholine was thus large, $9 to $93. Our best estimate of the cost per dose was $37. We conclude that the true cost per dose of succinylcholine from society's perspective is more than 20 times the acquisition cost. However, a precise costing requires better knowledge of the incidence and consequences of anaphylactic or anaphylactoid reactions to succinylcholine. IMPLICATIONS: The true cost of succinylcholine is more than 20 times the acquisition cost of the drug. The estimated cost is very sensitive to the risk and cost of patients dying or sustaining brain injury from anaphylactic or anaphylactoid reactions to succinylcholine.     

Volume replacement in acute anaphylactoid reactions

Two patients who experienced cardiovascular collapse due to anaphylactoid reactions are described. The first patient showed haemoconcentration which was rapidly restored with colloid solutions and vasoconstrictors. The second patient showed haemoconcentration in spite of massive infusion of crystalloid and repeated adrenaline; her circulatory status was restored with colloid solution. In acute anaphylactoid reactions both sympathomimetics and colloid solutions are necessary to restore circulation.     

Anaphylactoid reactions to contrast media which occurred during cholecystectomy and subsequent disseminated intravascular coagulation--a case report]

A 67-year-old woman without any history of allergic episode developed severe hypotension (40 mmHg) without skin rash one minute after the administration of amidotrizoic acid for intraoperative cholangiography during thoracic epidural and light general anesthesia. Although ephedrine, methoxamine, dopamine and norepinephrine were administered, severe hypotension persisted for three hours and epinephrine was only effective. Marked elevations of serum levels of histamine, leukotriene D4 and leukotriene E4 were noted after the episode, suggesting the occurrence of the anaphylactoid reaction to amidotrizoic acid and the activation of the immunological complement system. After the recovery from the anaphylactoid reaction, the patient developed disseminated intravascular coagulation (DIC) and severe bleeding around the wound for which reoperation was needed. It is necessary to consider some prophylactic treatments against DIC when severe anaphylactoid reaction occurred.     

Réaction anaphylactoide singulière après chlorure de succinyl-choline chez un enfant de 21 mois

An anaphylactoid reaction occurring after the intravenous administration of succinylcholine in a 21-month-old child is reported. The clinical manifestations and signs were limited to the upper airways and eyelids. The child was not known to be allergic or atopic. The IgE level was normal. The search for specific anti-choline IgE antibodies was negative. The skin tests were strongly positive for succinylcholine. The physiopathological and immunoallergic differences between anaphylaxis and anaphylactoid reaction are briefly discussed.     

Anaphylactoid purpura after intravesical therapy using bacillus Calmette-Guerin for superficial bladder cancer

We report a very rare side effect, anaphylactoid purpula, after intravesical administration of bacillus Calmette-Guerin (BCG). A 83-year-old man presented with purpura located on his bilateral lower legs. He had received transurethral resections four times for superficial bladder tumors. Intravesical therapy using BCG was performed. During the treatment course, asymptomatic purpura was suddenly seen in the lower legs after the third administration. Lymphocyte stimulation test was highly positive for BCG. He was diagnosed with anaphylactoid purpura caused by BCG. Conservative treatment was selected because there were no concomitant diseases in other organs. There have been no signs of recurrence of tumors or purpura during the one-year follow-up. However, physicians need to be cautious of anaphylactoid purpura which could lead to severe diseases, such as renal failure, gastrointestinal dysfunction and systematic arthritis.     

Anaphylactoid reaction to vecuronium followed by systemic reaction to skin testing

An unusual case is presented of a systemic anaphylactoid reaction to tubocurarine and subsequently to vecuronium. Intradermal testing with vecuronium following the latter response was negative at recommended test dose levels but at a higher concentration it initiated a hazardous systemic response. The laboratory investigations and possible mechanisms involved in this unusual case are discussed in detail since they may relate to other patients who experience anaphylactoid responses to anaesthetic drugs and who then undergo intradermal testing.     

Anaphylactic and anaphylactoid reactions

Anaphylactic and anaphylactoid reactions are an important area of anaesthesia and critical care medicine. Clinically they may be indistinguishable, and the immediate management for both conditions is identical. Immediate recognition and appropriate management are vital to prevent death. The aims of testing are to confirm an anaphylactic or anaphylactoid reaction, to identify the causative agent and to test for cross-reactivity with other related agents. Testing is complex and should be supervised by a clinical immunologist.     

Anaphylactoid reactions during anaesthesia

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.