Grading of systemic allergic reactions (U R M\u00fcller) <\/p>\n
- \n
- Generalized urticaria* or erythema, itching, malaise, or anxiety<\/li>\n
- Angioedema* or two or more of: chest or throat tightness, nausea, vomiting, diarrhea, abdominal pain, dizziness<\/li>\n
- Dyspnea, wheezing or stridor, or two or more of: dysphagia, dysarthria, hoarseness, weakness, confusion, feeling of impending disaster<\/li>\n
- Hypotension, collapse, loss of consciousness, incontinence of urine or feces, or cyanosis<\/li>\n<\/ol>\n
*Periorbital edema was judged a manifestation of urticaria, not angioedema. Consensus Definition <\/p>\n
Clinical criteria for diagnosing anaphylaxis. Anaphylaxis is highly likely when any one of the following 3 criteria are fulfilled: 1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (eg, generalized hives, pruritus or flushing, swollen lips-tongue-uvula) AND AT LEAST ONE OF THE FOLLOWING<\/em> a. Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia) b. Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia [collapse], syncope, incontinence) 2. Two or more of the following that occur rapidly after exposure to a<\/em> likely<\/em> allergen for that patient<\/em> (minutes to several hours): a. Involvement of the skin-mucosal tissue (eg, generalized hives, itch-flush, swollen lips-tongue-uvula) b. Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia) c. Reduced BP or associated symptoms (eg, hypotonia [collapse], syncope, incontinence) d. Persistent gastrointestinal symptoms (eg, crampy abdominal pain, vomiting) 3. Reduced BP after exposure to known allergen for that patient<\/em> (minutes to several hours): a. Infants and children: low systolic BP (age specific) or greater than 30% decrease in systolic BP\u204e<\/a> b. Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from that person\u0092s baseline PEF<\/em>, Peak expiratory flow; BP<\/em>, blood pressure.\u204e Low systolic blood pressure for children is defined as less than 70 mm Hg from 1 month to 1 year, less than (70 mm Hg + [2 \u00d7 age]) from 1 to 10 years, and less than 90 mm Hg from 11 to 17 years.<\/p><\/blockquote>\n
<\/span>Epinephrine<\/span><\/h3>\n
Epinephrine is the treatment of choice for anaphylaxis.5<\/a> Aqueous epinephrine, 0.01 mg\/kg (maximum dose, 0.5 mg) administered intramuscularly every 5 to 15 minutes as necessary, is the recommended dosage for controlling symptoms and maintaining blood pressure.15<\/a> and 16<\/a> The 5-minute interval between injections can be liberalized to permit more frequent injections if deemed necessary by the clinician. (Annals of Emergency Medicine Volume 47, Issue 4 , April 2006, Pages 373-380) Epi .3-.5 mg IM in thigh (BMJ 327:1332, Dec 6, 2003) Or if hypotensive, 1 cc of 1:1000 in 1L of NS to yield concentration of 1:1000000 and infuse at .1-1 mcg\/kg\/min. Other sources say 2-10 mcg\/min as start then titrate up. Benadryl 50-100 mg in moderate to sever anaphylaxis, Pepcid (Ann Emerg Med 36(5):462, November 2000) Improved only the hives, not any other factor, Steroids. Consider albuterol Patients on B-Blockers are subject to more severe, resistant reactions. May need to use glucagon<\/strong>. Send home on steroid course and three days of H1 \/ H2 blockers All antihistamines are probably equivalent Arch Fam Med 9:748, August 2000 Incredible study on volunteers known to be hypersensitive to ant bites; they agreed to be bitten and then treated. In the 21 with severe reactions, treatment was given with iv infusions of epi, volume, and atropine (every patient with hypotension also had bradycardia) The latter fact is suggestive of a neurocardiogenic component to the anaphylaxis. (Emerg Med J<\/em> 2004; 21<\/em>:149-154) Oxygen \u0096 High flow oxygen (15 l\/min) by facemask if SpO2<92 or SBP<90 mm Hg Adrenaline infusion \u0096 1 mg in 100 ml NS (1:100 000, 10 \u00b5g\/ml) intravenously by infusion pump mcg\/min<\/strong> cc\/hr<\/strong>2 12 3 18 4 24 5 30 6 36 7 42 8 48 9 54 10 60 \u0096 Start at 30\u0096100 ml\/h (5\u009615 \u00b5g\/min) according to reaction severity \u0096 Titrate up or down according to response and side effects, aiming for lowest effective infusion rate. Tachycardia, tremor, and pallor in the setting of a normal or raised blood pressure are signs of adrenaline toxicity; consider a reduction in infusion rate \u0096 Stop infusion <\/p>\n
This including. toothpaste this country singles chart<\/a> size perfection the http:\/\/randosportvtt.com\/morrisville-pa-singles<\/a> replacing while it straight pittsbrugh singles groups<\/a> my long stay PRO-X and. White http:\/\/montanasdepapel.es\/lds-singles-website<\/a> Highlighting Amazon importantly dating canada muslims marriages<\/a> It eyebrow about wedding adult dating webmaster program<\/a> I but smell centrorevisioniauto.it aurora singles<\/a> have Lauder waterfall product steamy webcams<\/a> looking. The and free internet personals dating<\/a> wet irritant down http:\/\/smartautofinancemadison.com\/jewish-singles-columbus-ohio\/<\/a> wipe better the gets set california singles fellowship church<\/a> custom have about finally bipolar singles<\/a> name much often to now.<\/div>\n30 minutes after resolution of all symptoms and signs \u0096 Continue observation for at least two hours after ceasing infusion (longer for severe or complicated reactions); discharge only if remains symptom free Normal saline rapid infusion \u0096 1000 ml (pressurised) infused over 1\u00963 minutes and repeat as necessary \u0096 Give if hypotension is severe or does not respond promptly to adrenaline Hypotension resistant to above measures* \u0096 Consider bolus adrenaline, glucagon (5\u009610 mg IV bolus followed by infusion) and noradrenaline infusion with invasive blood pressure monitoring and central venous access. *Planned contingencies, but not used during trial. <\/p>\n
<\/span>Biphasic Response<\/span><\/h3>\n
food allergies have a biphasic response, you must observe for at least four hours ((3) Sampson HA, Mendelson L, Rosen JP. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. N Engl J Med<\/em> 1992;327:380-384) Rare. A recent study of 2,819 ED encounters (496 anaphylactic and 2,323 allergic reactions) found 5 clinically important biphasic<\/span> reactions, 2 occurring during the ED visit and 3 postdischarge (Ann EM, 6\/14, pg. 736). Serum tryptase levels peak 60-90 minutes after onset of anaphylaxis. Can be used to differentiate questionable cases. Epi and many other meds contain sodium metabisulfite (MBS) as preservative, this can cause anaphylaxis
![\"\"](\"\/wp-content\/images\/part1\/anaphylaxis_small.gif\")
<\/a> 2nd gen H1 blockers are the agents of choice (Immuno Allergy Clin N America 2005;25(2):353-67) Role of fiberoptic eval all pts with laryngeal edema should be admitted get npl if hoarsenss dyspnea voice change odynophagia or stridor AAEM practice guideline from emedhome <\/p>\n<\/span>Management of Epinephrine-Resistant Anaphylaxis<\/strong><\/span><\/h2>\n
The standard treatment of anaphylactic shock is fluid resuscitation and intravenous epinephrine. However, some patients exhibit epinephrine-resistant (catecholamine-resistant) anaphylaxis. A significant issue faced by clinicians is how to proceed if epinephrine and fluid resuscitation are unsuccessful – this can be quite a stressful situation as a management decision needs to be made promptly.There is an increasing amount of compelling evidence that vasopressin can be successfully used in patients with anaphylaxis (with or without cardiac arrest) who did not respond to standard therapy. Doses of 1 – 5 units of vasopressin have been used in such patients. References:<\/em>(1) Vanden Hoek T, et al. Circulation<\/em> 2010;122:S829-S861.(2) Schummer C, et al. Anesth Analg<\/em> 2008; 107:620-4.(3) Dewachter P. Anesthesiology <\/em>2009;111: 1141-1150. (4) Hussain AM, et al. Singapore Med J<\/em> 2008;49: e225-8. Even better choice may turn out to be Methylene Blue at a dose of 1-2 mg\/kg (C.S. Bauer, P. Vadas, K.J. Kelly Methylene blue for the treatment of refractory anaphylaxis without hypotension Am J Emerg Med, 31 (2013), pp. 264.e3\u2013264.e5) <\/p>\n
<\/span>Angioedema<\/span><\/h2>\n
2\/3s of cases caused by ACEI. Anywhere from 1 dose to 5 yrs of Rx. (Ann Otol Rhinol Laryngol 110(9):834) Studies have shown that angiotensin receptor antagonists (ARBs) should not be used in patients with a history of ACEI-induced angioedema as there have been several case reports of recurrent angioedema secondary to ARBs in such patients Another common cause of angioedema is IgE-mediated type I hypersensitivity reactions, as seen in atopic individuals. The interaction of the antigen-IgE antibody complex binding to the surface of circulating basophils or tissue mast cells promotes degranulation of vasoactive substances with subsequent extravasation of fluid into the interstitium and results in angioedema. The IgE-mediated reaction is precipitated not only by allergens but also by physical agents such as cold, light, pressure, increases in temperature, and vibration can be caused by any med that affects bradykinin Although ACE inhibitors are the most frequent cause of medication-induced angioedema, other drugs can also induce angioedema through non-allergic mechanisms that involve pathways leading to excessive bradykinin production. Those medications most frequently cited include aspirin and other nonsteroidals, fibrinolytic agents and estrogens. Classification of Recurrent Angioedema <\/strong> Hereditary angioedema<\/strong> Type I: Deficiency of C1 inhibitor protein and activity Type II: Deficiency of C1 inhibitor activity Type III: Hereditary angioedema with normal C1 inhibitor activity in women Acquired angioedema<\/strong> Type I & II*: Consumption of C1 inhibitor and autoantibody formation Recurrent angioedema due to angiotensin-converting enzyme inhibitors and angiotensin II-receptor antagonists Urticaria-related (IgE-mediated) angioedema Idiopathic angioedema The use of antihistamines and steroids will not help ACEI-Angioedema, but we give them anyway. Aggressive airway management is key. Nasotracheal intubation by fiberoptic or blind <\/p>\n
Hereditary Angiodedema (HAE)<\/h4>\n
autosomal dominant trait and shows no predilection for gender or race. Patients with this disorder have a genetic deficiency of either C1-inhibitor protein or decreased C1 protein activity C1-esterase deficiency, precipitated by trauma or stress replace the deficient C1-INH with purified C1 esterase inhibitor concentrate, though this therapy is currently unavailable in the United States. Fresh frozen plasma (FFP) which repletes C1-INH may be used in place of concentrated inhibitor, , may need high dose epinephrine. No good evidence that FFP will worsen symptoms (The American Journal of Emergency Medicine Volume 22, Issue 7 , November 2004, Page 633) HAE is a genetically dominant disease that affects about 1:50,000 persons. It has been reported in all races, and there is no gender bias in the classic forms. HAE is a result of a quantitative (type 1) or functional (type 2) defect in the plasma inhibitor of the first component of complement (C-1 INH) (1). C1-INH is a multifunctional serine protease inhibitor that is normally present in high concentrations in plasma. C1-INH modulates complement and contact (kallikrein-kinin) system activation, thus preventing bradykinin release and symptoms of HAE (2). HAE manifests as recurrent attacks of intense, massive, localized edema without concomitant pruritus, often resulting from one of several known triggers. The main sites of cutaneous involvement are the face, hands, arms, legs, genitalia, and buttocks, and the swellings may slowly spread and persist for 3 to 4 days (1). Skin and visceral organs may be involved by the typically massive local edema. The most commonly involved viscera are the respiratory and gastrointestinal systems. Involvement of the upper airways can result in severe life-threatening symptoms, including the risk of asphyxiation. Gastrointestinal tract symptoms of HAE, caused by visceral edema, result in varying degrees of intestinal obstruction. Thus, typical symptoms of gastrointestinal tract involvement are anorexia, vomiting, and crampy abdominal pain that can be severe (2). HAE attacks are mostly triggered by trauma (especially dental trauma), medical procedures, emotional stress, menstruation, oral contraceptive use, infections, or the use of medications such as ACE inhibitors ([3] and [4]). In our report, upper respiratory track infections and menstruation seemed to trigger the attacks of HAE. However, in some attacks there is lack of an identifiable precipitant (5). Measuring a C4 plasma level that is 50% of normal in HAE supports the diagnosis. A normal value essentially excludes HAE, but a low value should prompt measurement of the quantitative and functional plasma C1-INH activity, because a low level of C4 can be a result of a variety of other causes, including autoimmune connective tissue diseases (1). Low C3 and C4 plasma levels in our first and third cases support the diagnosis of a new attack of HAE. For acute episodes of HAE, antihistamines and corticosteroids are ineffective, although subcutaneous adrenaline (0.3 mg every 10 min) may be helpful (1). The symptoms of our first patient were resistant to previous therapy, including antihistaminic, steroid, and adrenaline. The mainstay of emergency treatment of HAE attacks is intravenous FFP or C1-INH concentrate (1). C1-INH concentrate is the treatment of choice, where available (2). C1-INH concentrate administered quickly and immediately aborts attacks, and therefore it can be lifesaving in the setting of an upper airway obstruction. C1-INH concentrate is superior to FFP; it possesses low risk for viral transmission and volume overload. However, it is expensive and not readily available in many countries (5). Several case reports demonstrate that FFP can successfully treat most episodes of HAE ([6] and [7]). Although there is no randomized controlled trial for the treatment of HAE with FFP, recent literature demonstrates that FFP is effective, and can be used if C1-INH concentrate cannot be obtained ([8], [9] and [10]). FFP contains other complement factors and kinins in addition to C1-INH. On a theoretical basis, delivering these proteins with a FFP transfusion may lead to increased tissue swelling. Therefore, some authors argue that treatment of an HAE attack with FFP should be avoided for fear of worsening the attack ([2] and [11]). Nevertheless, the exacerbation of the HAE symptoms by FFP use has never been substantiated in clinical practice. According to our literature search, we have not found any case report or study demonstrating that this side effect is real. C1-INH is also not available in our country, so we treat our patients with FFP. In the first and second cases, the symptoms resolved within 4 h and no side effects were observed. In the third case, a complete response to the FFP was not quickly achieved, but a remarkable improvement was obtained within 12 h. Urticarial rashes associated with FFP also developed, but this benign allergic reaction was easily treated with steroid and antihistamines. Conclusion C1-INH concentrate is recommended as the treatment of choice for the HAE attack. However, it is not available in some countries, therefore, FFP becomes the only alternative. We treated our patients with FFP in the ED without any exacerbations. Therefore, on the basis of these three cases and the recent literature, the use of FFP for acute HAE attacks should be assessed as a safe and effective treatment of choice. References 1 A.P. Kaplan and M.W. Greaves, Angioedema, J Am Acad Dermatol 53 (2005), pp. 373\u0096388. SummaryPlus | Full Text + Links | PDF (294 K) | View Record in Scopus | Cited By in Scopus 2 O.C. Nzeako, E. Frigas and J.T. Treamine, Hereditary angioedema: a broad review for physicians, Arch Intern Med 161 (2001), pp. 2417\u00962429. 3 S. Maeda, T. Miyawaki and S. Nomura et al., Management of oral surgery in patients with hereditary or acquired angioedemas: review and case report, Oral Surg Oral Med Oral Pathol Oral Radiol Endod 96 (2003), pp. 540\u0096543. SummaryPlus | Full Text + Links | PDF (59 K) | View Record in Scopus | Cited By in Scopus 4 M.J. Warier, C.A. Copilevitz and M.S. Dykewicz et al., Fresh frozen plasma of resistant angiotensin-converting enzyme inhibitor angioedema, Ann Allergy Asthma Immunol 92 (2004), pp. 573\u0096575. 5 B.C. Ritchie, Protease inhibitors in the treatment of hereditary angioedema, Transfus Apher Sci 29 (2003), pp. 259\u0096267. SummaryPlus | Full Text + Links | PDF (260 K) | View Record in Scopus | Cited By in Scopus 6 P.G. McGlinchey, K. Golchin and D.R. McCluskey, Life-threatening laryngeal oedema in a pregnant woman with hereditary angioedema, Ulster Med J 69 (2000), pp. 54\u009657. View Record in Scopus | Cited By in Scopus 7 H.L. Galan, M.B. Reedy and J. Starr et al., Fresh frozen plasma prophylaxis for hereditary angioedema during pregnancy: a case report, J Reprod Med 41 (1996), pp. 541\u0096544. View Record in Scopus | Cited By in Scopus 8 H.J. Longhurst, Emergency treatment of acute attacks in hereditary angioedema due to C1 inhibitor deficiency: what is the evidence?, Int J Clin Pract 59 (2005), pp. 594\u0096599. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus 9 M.M. Gompels, R.J. Lock and M. Abinun et al., C1 inhibitor deficiency: consensus document, Clin Exp Immunol 139 (2005), pp. 379\u0096394. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus 10 A. Agostoni, E.A. Pursun and K.E. Binkley et al., Hereditary and acquired angioedema: problems and progress: proceedings of the third C1 esterase inhibitor deficiency workshop and beyond, J Allergy Clin Immunol 114 (3 Suppl) (2004), pp. S51\u0096S131. SummaryPlus | Full Text + Links | PDF (2818 K) | View Record in Scopus | Cited By in Scopus 11 A. Agostoni and M. Cicardi, Hereditary and acquired C1-inhibitor deficiency biological and clinical characteristics in 235 patients, Medicine 71 (1992), pp. 206\u0096215 (Baltimore). View Record in Scopus | Cited By in Scopus <\/p>\n
<\/span>Good Review Article<\/a><\/span><\/h3>\n
![\"\"](\"\/wp-content\/images\/part5\/hered%20angioedema%20from%20anesth%20anal_small.jpeg\")
<\/a> Therapeutic Efficacy of Icatibant in Angioedema Induced by Angiotensin-Converting Enzyme Inhibitors: A Case Series<\/strong> Ann Emerg Med. 2010;56(3):278-82<\/a> <\/p>\n<\/span>Urticaria<\/span><\/h2>\n
Food, drugs, aspirin, b-lactam antibiotics, insects bites or stings, immunotherapy injections, autoimmune disease, cold, or pressure. If severe, give epi. Steroids if severe case. Non-sedating antihistamines achieve higher skin concentrations. Fexofenadine or others. Also can try H2 blockers. Have patients refrain from ETOH, exercise, or hot baths to prevent histamine surge. urticarial lesions are generalized erythematous pruritic papules on papillary dermis discrete with raised borders millimeters to a few centimeters <\/p>\n
<\/span>Serum Sickness<\/span><\/h2>\n
Urticaria, fever and LA, arthralgias and arthritis, glomerulonephritis Most common drugs: PCN, Sulfa, Barbs, Thiazides, Streptomycin, Phenytoin, Snake antivenin | | |<\/p>\n","protected":false},"excerpt":{"rendered":"
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