anaphylaxis
Post on 22-May-2015
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Pathophysiology & Management
Scott Cooper B.Sc. (Hons.) Dip. Paramedical Science
Understanding the terminology
Pathophysiology
Signs and Symptoms
Clinical Management
Understanding the terminology
Pathophysiology
Signs and Symptoms
Clinical Management
Between 1996 and 2007 there where 112 anaphylaxis fatalities in
Australia
During those 9 years, food induced anaphylaxis admissions
increase by 350%
Globally, the incidence of allergic related medical conditions
related to food allergies is on the rise
In the US there are approximately 150-200 anaphylaxis death
annually
Hospital admission for anaphylaxis management have increased 7 x
in the last decade in the UK
Between 1996 and 2007 there where 112 anaphylaxis fatalities in
Australia
During those 9 years, food induced anaphylaxis admissions
increase by 350%
Globally, the incidence of allergic related medical conditions
related to food allergies is on the rise
In the US there are approximately 150-200 anaphylaxis death
annually
Hospital admission for anaphylaxis management have increased 7 x
in the last decade in the UK
AnaphylaxisCan be defined as “An exaggerated immune
response to a foreign antigen or protein resulting in severe life threatening condition”
Refers to the physiological events regardless of activation mechanism.
The term was first used by a couple of FRENCH scientists who where abusing dogs by testing sea anemone antivenin on cute little beagle puppies with sad eyes. It was noted that one of the dogs died without a perceived reason.
Anaphylaxis continued
Aetiologies are grouped into either:
Allergic Mediated by Immunoglobulin E (Ig-E) Require previous exposure and sensitization The most common trigger of anaphylaxis
Non allergic or anaphylactoid Conflicting evidence as to whether these reaction are
activated by IgE response or not No previous exposure or sensitization required
Anaphylactic Shock
Shock can be defined as a state of poor systemic perfusion
Anaphylactic shock is a state of poor end organ perfusion as a direct result of the anaphylactic reaction
In summary anaphylactic shock is just one of many possible clinical manifestations resulting from a severe allergic reaction.
Basophils
A type of granulocytic white blood cellMake up <1% of WBC countAlthough able to initiate release of
chemical weapons, also possess the ability to initiate mast cells to trigger
Predominantly secrete histamine when triggered.
ARE MOBILE!
Mast Cells
Similar to basophils, these cells are located throughout the body bound in connective tissue.
Concentrated beneath the skin and the mucous membranes of the respiratory and digestive tracts
Can be considered as storage points for chemical WMD’s
When activated, release a multitude of chemical inflammatory mediators
Sensitisation
Joe Boggs aged 2 eats his first ever peanut. Certain cells called blah blah blah cells, for some reason, believe this protein to be foreign and dangerous
Blah blah blah cells take photographs of the protein and take it to the bling bling cells who produce massive quantities of an antibody type, IgE. This antibody is specific to these proteins.
The IgE antibodies bind to mast cells and basophils, ready to attack if this protein shows up again
Stage One
Joe Boggs aged 2 and 26 days eats his second ever peanut.
As soon as the protein is absorbed into the blood stream, circulating basophils detect the presence of this recognised foreign antigen invader.
All hell breaks loose and a cascade of highly complex biochemical pathways result in the basophils screaming “CODE RED!!”
The basophils flow throughout the blood stream, releasing their chemical weapons as they go, if they haven't already been triggered by the same protein, they also get their bigger mates, the Mast Cells to fire their weaponry as well
Stage TwoBasophils now initiate what is known as a ‘Mast cell-leukocyte-cytokine-cascade
In normal people, this reaction is controlled by a feedback system ensuring the cascade does not get out of hand.
In persons with a SAR, this process becomes uncontrolled and results in the release of multiple chemical mediators over seconds, minutes and hours
Stage ThreeDisseminated mast cell activation
release a variety of noxious mediators including:HistaminesProstaglandinsLeukotriensChemokinesCytokines
These rapidly synthesized toxic compounds elicit a widespread increase in vascular permeability and vasodilatation
Stage FourThe patient begins to feel unwell as the
inflammatory mediators act on the target tissues
The integumentary, cardiovascular, respiratory, gastro intestinal and central nervous systems can all be affected.
If the patient has integumentary involvement (Urticaria, erythema, swelling or pruritis (itching)) AND Respiratory compromise OR hypotension, the patient is said to be in anaphylaxis
Integumentary SystemDue to the high concentration of mast
cells under the skin, this is often the first sign of an impending reaction
Histamine causes vasodilatation of the micorcapillaries resulting in a flushed appearance
As the capillaries become more permeable, plasma leaks into the interstitial space resulting in urticaria and pruritis due to the irritation of plasma being outside of the vessel wall
Cardiovascular SystemInflammatory mediators including
histamine, Leukotriens and kinins now cause widespread vasodilatation and vessel wall permeability,
As much as 35% of circulating fluid volume can be lost to the interstitial space, this coupled with the massive vasodilatation causes a rapid drop in blood pressure, anaphylactic shock.
Baroreceptors in the aortic arch and carotid bulb detect this pressure drop and heart rate increases.
Cardiovascular System (cont’d)As the blood pressure drops, pre load and
after load decrease, resulting in a potential for poor cardiac perfusion, this is of particular concern in the elderly or patients with cardiac disease.
As the fluid builds up in the interstitial spaces, angioedema begins to cause swelling, particularly to the eyes, ears, mouth and tongue, throat and lungs
The patient begins to complain of a lump or itching in throat, dysphagia and dyspnoea as the upper airway / tongue swells.
Severe Glossal Oedema
Angelina Jolie or Angiodema…..
Laryngoscope View of Laryngeal oedema
Respiratory SystemAs well as previously discussed upper
respiratory tract inflammation due to angioedema, the smooth muscle of the distal bronchi also constrict, causing a reduction in the lumen diameter, resulting in further airflow resistance. This is a futile protection mechanism to limit the exposure to the antigen
As the patient becomes hypoxaemic, the respiratory rate increases dramatically
Hypoxaemia leads to further vasodilatation and tachycardia, placing more strain on the heart.
GastrointestinalMost gastrointestinal symptoms are due
to the release of serotonin during the reaction, this the bowel to spasm, causing abdominal cramping, induces nausea and diarrhoea.
This is an attempt by the body to rid itself of the antagonist, by increasing bowel transit and inducing vomiting.
Strong GI symptoms have been associated with an increase in severity and incidence of anaphylaxis.
Central Nervous SystemMost CNS symptoms are due to
hypotensionExpect anxiety, dizziness, confusion, and
often combative behavior as cerebral blood flow is compromised
ANY GCS less than 15 indicates poor cerebral perfusion and is time critical.
Most patients experiencing hypotension genuinely believe they are dying, rest and reassurance is an essential aspect of patient management
Primary Survey DRABC find and fix Airway
Adrenaline to reduce and arrest the laryngeal / glossal oedema
BreathingHigh flow Oxygen, slow gentle IPPV if requiredBronchodilators to assist with bronchospasm
CirculationRAISE THE LEGS! Simple but highly effectiveFluids to maintain end organ perfusionAdrenaline to increase vascular tone
Treatment depends on the symptomsPrepare for the worst i.e. cardiac arrest
It should be remembered that anaphylaxis can be Monophasic, Biphasic or multiphasic
Most people recover immediately after aggressive intervention without experiencing further symptoms, some however do, as much as 24 hours later.
Always transport patient for physician assessment, never leave a patient at home following anaphylaxis, even if asymptomatic
ADRENALINEAdrenaline is a naturally occurring catecholamine which primarily
acts on Alpha1 and Beta1 & 2 adrenergic receptors, located mainly in tissues innervated by sympathetic nerves.
(1) increases heart rate Increases the force of myocardial contraction Increases the irritability of the ventricles
(2) Bronchodilation
(1) Peripheral vasoconstriction
ADRENALINE (cont’d)
There is also anecdotal evidence that adrenaline assists in stabilising the mast cells from degranulating
The net results of adrenaline are: Increase in vascular tone Increase in BP Increase in preload and afterload Decrease in vascular permeability Decrease in swelling Acts as a bronchodilator
ADRENALINE (cont’d)
Whilst it is important adrenaline is administered in a timely fashion for patients in anaphylaxis, it is also prudent to consider the following: Adrenaline can be a dangerous drug! Is this a genuine anaphylaxis (Vasovagal? or anxiety??)
Consider age and cardiac health of patient in dosing
Best Route IMI (vastus lateralus as more reliable absorption profile) Nebulised (for isolated minor facial and/or tongue swelling thought to be
allergic in origin – IMI if stridor present)
Ensure adequate monitoring of patient post administration
ADRENALINE (cont’d)
ADULT I.M.I. = 250 - 500mcg every 5 minutes until Pt stabilises
Consider age of patient, medical condition of patient and severity of reaction
Nebulised = 5mg, single dose
PAEDIATRIC I.M.I. = 10mcg / kg (Max 250mcg) every 5 minutes until Pt
stabilises for patients equal to or >1 years of age I.M.I. = 100mcg every 5 minutes until Pt stabilises for patients
equal to or <1 years of age Nebulised = 5mg, Single dose
ADRENALINE (cont’d)
EpiPen Most people identified as having high risk to anaphylaxis are
provided with an EpiPen If already administered, dose should be taken into account Below table shows the standard dose of EpiPen in Australia
WeightWeight EpiPen DoseEpiPen DoseChildren < 10kgChildren < 10kg Not usually RecommendedNot usually Recommended
Children 10-20kgChildren 10-20kg EpiPen Jr. 150mcgEpiPen Jr. 150mcg
Children & Adults >20kgChildren & Adults >20kg EpiPen 300mcgEpiPen 300mcg
Fluids
Severely shocked patient require large volumes of a suitable crystalloid solution to maintain organ perfusion!
Adrenaline is the first line drug but fluids also have a vital role to play, and may in fact be the only and / or safer intervention required
2-3 litres rapid infusion through at least a 16g is recommended for hypotensive patients, consider
Bronchodilators e.g. Salbutamol
The respiratory symptoms exhibited by patients in anaphylaxis are very similar to those exhibited by asthmatics.
Smooth muscle constriction may be relieved by bronchodilators such as salbutamol
Salbutamol sulphate is a direct acting sympathomimetic agent which mainly effects β2 receptors. As a predominantly β2 adrenoreceptor stimulant, Salbutamol bronchodilating action is relatively more prominent than its cardiac effects
Anti Histamines
Generally not recommended for serve allergic reactions Histamine is just one of the many inflammatory mediators
responsible for initiating anaphylaxis and is more of an initial mediator than a protracted one.
Histamine has been shown to peak early and then return to normal despite the persistence of severe physiological compromise
The main issue of concern is that the major antihistamine promethazine (phenergan) is a vasodilator and may in fact worsen the patients outcome.
It would therefore seem prudent that phenergan be restricted to the treatment of skin symptoms and not in patients with realised or potential haemodynamic compromise
Steroids
Inhibit the accumulation of inflammatory cells at inflammation sites
Inhibits the release and synthesis of inflammatory mediators
Plays a part in suppressing cell mediated immune reactions
Glucagon
Glucagon is a hyperglycemic agent but it also acts as a poor mans adrenaline in beta blocked patients!
If a patient is beta blocked the efficacy of adrenaline may be severely reduced due to it’s inability to bind to the beta receptor sites
Glucagon works by binding to a different receptor site but still elicits similar effects as adrenaline within the cell.
Recommended dose = initial load of 1-5mg I.V.I. over 5 minutes
NOT RECOGNISED QAS MANAGEMENT, JUST FOR INTEREST
Useful questions to ask your patient:Do you suffer from any of the following?
AsthmaBad hay feverSevere allergies
Remember these patient groups are statistically more likely to experience and anaphylactic reaction
Are you taking beta blockers?May explain why adrenaline isn’t working!
Familiarise yourself with adrenaline regularly: When to give itDosagesHow to draw that dose up, How to administer it safely IMI (aspirate)The risks associated with it
Although anaphylaxis is rare, you never know when you might need it!
Journal of Emergency medicine July 2002 Anaphylaxis
Emergency Medicine Australia 2006 Anaphylaxis: Clinical concepts and research priorities
Allergy Notes August 2008 Anaphylactoid Reactions to Intravenous Contrast media
New England Journal of Medicine November 2006 Anaphylaxis Prevention via pretreatment
Emergency Care in the Streets Nancy Caroline Queensland Ambulance Service Clinical Protocol Manual Drug Therapy protocols
Ultravist Drug information Guide And many more!!!!!!!
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