ANAPHYLAXIS EMET 2015
ANA = AGAINST PHYLAX = PROTECTION No standardised definition (they re working on it) All include the similar concept of: A serious, generalised or systemic, allergic or hypersensitivity reaction that can be life-threatening or fatal.
CLINICAL FEATURES OR
The correct term anaphylaxis is preferred to anaphylactic shock because shock is not necessarily present in patients with anaphylaxis. The term anaphylaxis should also be used in preference to terms such as: allergic reaction acute allergic reaction systemic allergic reaction acute IgE-mediated reaction anaphylactoid reaction pseudo-anaphylaxis
HOW COMMON IS IT? Uncommon but not rare. Under-recognised and under-treated. Lifetime prevalence 0.05-2% Prevalence is increasing ED death rate 1 per 100-200 presentations A parent-reported survey found 1 in 170 Australian school children had suffered at least one episode In south-eastern Australia, 1 in 50 adults have experienced anaphylaxis after stings from native Myrmecia species or honeybees
JACK JUMPER ANT Myrmecia pilosula
COMMON CAUSES Insect stings: most commonly honeybees, Australian native ants, wasps Foods: most commonly peanuts, tree nuts, egg, seafood, cows milk, dairy products, seeds Medications: most commonly antibiotics, NSAIDs Idiopathic (no cause found)
In ED studies where the cause has been identified: food allergy is responsible for about 80% of anaphylactic reactions in children but only 20-30% of cases in adults This is reflected in the median ages for lethal reactions: to foods = 22 24 years to insect venoms or medications = 55 67 years,
LESS COMMON CAUSES Physical triggers (eg, exercise, cold) Biological fluids (eg, transfusions, immunoglobulin, antivenoms, semen) Latex Dialysis membranes (haemodialysis-associated anaphylaxis) Hydatid cyst rupture Aeroallergens: domestic/laboratory animals, pollen Tick bites Hormonal changes: breastfeeding, menstrual factors Food additives: MSG, metabisulfite, preservatives, colours, natural food chemicals Topical medications (eg,
SUMMATION ANAPHYLAXIS Cofactors are sometimes required before an allergen will provoke a reaction. Factors associated with increased risk of anaphylaxis include: intercurrent infection concomitant medication (particularly alpha-blockers, beta-blockers, ACE inhibitors, NSAIDs) foods (particularly alcohol, and spicy food) high ambient temperatures exercise - predominantly affecting young adults This may explain intermittent anaphylaxis despite frequent allergen exposure, and may account for some idiopathic cases. Some individuals experience symptoms with exercise alone; others do so only if allergenic foods are ingested within a few hours prior to exercise.
MAST CELL OR BASOPHIL ACTIVATION Immunological cascade
MUCOCUTANEOUS Rhinitis Conjunctival erythema and tearing Flushing Itch Urticaria Angioedema
ABDOMINAL / PELVIC Nausea Vomiting Abdominal pain Pelvic pain (described as being like uterine contractions ) Delayed vaginal discharge
NEUROLOGICAL Vascular headache (typically described as throbbing ) Dizziness Collapse, with or without unconsciousness Confusion Incontinence
RESPIRATORY Dysphagia and stridor due to upper airway angioedema Throat and/or chest tightness Dyspnoea Cough Wheeze Cyanosis
CARDIOVASCULAR Palpitations Tachycardia Bradycardia (relative or absolute) ECG changes (T and ST changes) Hypotension Cardiac arrest
DEATH The predominant shock organs in anaphylaxis are the heart, lung, and vasculature. Fatalities are divided between circulatory collapse and respiratory arrest. Heart: myocardial depression, arrhythmias, and ischemia. Contributing factors include direct mediator effects on the myocardium, exacerbation of preexisting myocardial insufficiency by the hemodynamic stress of anaphylaxis, and exogenous or endogenous epinephrine. Respiratory tract: bronchospasm and mucus plugging in the smaller airways, and laryngeal edema and asphyxiation in the upper airway. Asphyxiation typically occurs rapidly after allergen exposure, with death occurring within one hour in many cases. Severe bronchospasm during anaphylaxis characteristically develops in individuals with preexisting asthma. During anaphylaxis, peripheral tissues continue to consume oxygen at relatively high rates. This, in combination with peripheral vasoconstriction and decreased perfusion, leads rapidly to anaerobic metabolism and end-organ damage.
PHASIC RESPONSES Uniphasic anaphylaxis 80-90% of all episodes. Usually peaks within 30min -1hr after symptoms appear and resolves either spontaneously or with treatment within the next 30min - 1hr. Biphasic anaphylaxis 1-23%. Characterized by a uniphasic response, followed by an asymptomatic period of an hour or more, and then a subsequent return of symptoms without further exposure to antigen. Studies are conflicting as to the severity and significance of second reactions. Fatalities have been reported. Risk factors have not been established. Protracted anaphylaxis Lasts hours to days without clearly resolving completely. Uncommon
TREATMENT 1. Stop exposure to the causative agent. 2. Call for assistance. 3. IM adrenaline to lateral thigh 0.5mg (0.01mg/kg) 4. Lay patient flat (elevate legs if tolerated) 5. Give high flow O2 + airway/ventilation support if needed. 6. Get IV access.
IF HYPOTENSIVE Give normal saline bolus 20ml/kg over 1-2 mins (max 50ml/kg in first 30 mins) Insert second IV line Significantly more adrenaline is likely to be required. Hypotension is usually accompanied by a relative bradycardia, (esp. sting anaphylaxis) - add Atropine.
IF INADEQUATE RESPONSE Repeat IM adrenaline every 3-5 mins or Start IV adrenaline infusion CAUTION - IV boluses of adrenaline are not recommended
IF UPPER AIRWAY OBSTRUCTION Continue adrenaline IM or infusion Give nebulised adrenaline 5 x 1mL amps Consider intubation
FOR PERSISTENT WHEEZE Salbutamol 12 puffs via spacer or 5mg neb Prednisolone 50mg (1mg/kg) PO or Hydrocortisone 200mg (5mg/kg) IV
ANTIHISTAMINES? Antihistamines have no role in treating respiratory or cardiovascular symptoms of anaphylaxis. Oral non-sedating antihistamines may be given to treat itch and urticaria. Injectable promethazine should not be used in anaphylaxis as it can worsen vasodilation and hypotension.
STEROIDS? Commonly given, but no evidence to support this May be useful if wheeze is persistent and in patients who are also asthmatics. Recent large retrospective study showed oral steroids had no effect: did not prevent clinically significant biphasic relapses did not decrease ED representations
ONCE THE DUST HAS SETTLED Observation Confirming the diagnosis Long-term management
HOW LONG TO OBSERVE? At least 4 hours after last dose of adrenaline. Observe longer (overnight) if patient: had a severe reaction (hypotension or hypoxia) required repeated doses of adrenaline has a history of asthma or protracted anaphylaxis has other concomitant illness lives alone or is remote from medical care
WAS IT ANAPHYLAXIS? >40 potential symptoms. Wide differential. Not always obvious. Consider an allergic cause in any acute onset urticaria or angioedema lasting <12 hours. Skin signs are missing in 20% of cases. Consider it in the differential for any case of acute respiratory distress, brochospasm, or cardiovascular collapse.
Retake the history while it is still fresh: Exposures in the past 8 hours, cofactors, occupational, food, meds Ask patients about symptoms of contact urticaria (eg, during food preparation) or itching in the mouth and throat after eating certain foods (oral allergy syndrome). Sting anaphylaxis occurs within 1 hour. Food anaphylaxis occurs within 6 hours.
INPATIENT INVESTIGATIONS Not helpful for management of the acute presentation but can confirm that anaphylaxis did occur. Serum tryptase levels (elevated in 60%) within 3 hours of onset and again at 4-6 hours. Plasma histamine levels within 1 hour of onset.
OUTPATIENT INVESTIGATIONS In vitro testing for allergen-specific IgE: a useful screening test for a variety of allergens RAST or ImmunoCAP Pitfalls: lacks sensitivity limited by the range of allergens available can only claim Medicare rebates for four allergens at a time. measurement of total IgE and in-vitro testing using food mixes frequently provide misleading or irrelevant results and should not be requested.
In vivo - Skin prick testing: to assess sensitisation to food, medications, or insect venom more sensitive than in-vitro testing. Pitfalls: small risk of inducing anaphylaxis should only be carried out in an environment in which resources for treating anaphylaxis are available. Skin testing for jack jumper ant allergy is not yet available outside the Royal Hobart Hospital.
Some drug reactions (eg, to NSAIDS, radiographic contrast agents) are independent of IgE, and there are numerous difficulties in assessing some cases of antibiotic allergy. To establish a diagnosis in cases in which the causative agent is in doubt, challenge testing under controlled conditions may sometimes be required, although a negative challenge test does not always exclude the diagnosis. There is no scientific validity for alternative therapies such as cytotoxic or Vega testing, hair analysis, or kinesiology, and their use should be discouraged.3
WHEN TO REFER? Specialist evaluation is recommended after a diagnosis of possible anaphylaxis: to identify or confirm the cause to educate regarding appropriate avoidance strategies to help in drafting an emergency action plan to advise whether immunotherapy is appropriate
LONG TERM MANAGEMENT Long-term risk reduction includes the following elements: Ongoing education about recognition and prompt treatment of future anaphylactic episodes Optimal management of relevant comorbidities (eg, asthma or cardiovascular disease) and assessment or reassessment of the benefits and risks of concurrent medications, eg, beta-blockers or ACE inhibitors Strict avoidance of specific relevant triggers Specific interventions to reduce or prevent anaphylaxis recurrences from some triggers (examples include venom immunotherapy for those with anaphylaxis from stinging insects, and desensitization for those with anaphylaxis from some medications)
PATIENT EDUCATION POINTS Recognition of the symptoms and signs. The severity of a previous episode does not reliably predict that of future episodes. How to use an Epipen/Anapen. Taking responsibility for own adrenaline supply. Playing down the role of antihistamines / salbutamol.
AUTO-INJECTORS
DISCHARGE PACKAGE Action plan Specialist referral Adrenaline training - may need several doses if they live remotely. EpiPen expires after 6 months. Put an alert on the patient s file Medical alert bracelet Management of comorbidities / medications.