Anaphylaxis Management During Procedural Sedation

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Introduction
Anaphylaxis is a medical emergency that requires immediate recognition and intervention. Equipment and medication should be readily available. Early administration of adrenalin is the key to survival. In this paper we
discuss the critical aspects of anaphylaxis: the definition, presentation, the pathophysiology, the best emergency management and measures to prevent recurrence.
Keywords: anaphylaxis, adrenaline, laryngeal edema,
emergency management, procedural sedation
Discussion
Anaphylaxis is a severe, life-threatening, systemic hypersensitivity reaction that is immunologically mediated.1 This unpredictable syndrome involves multiple organs as a result of the sudden systematic release of mast cells and basophil mediators.2 Nothing should delay the early administration of intra-muscular adrenaline as this is the
key to a successful outcome.1 Many definitions, criteria and terminology exist for
anaphylaxis. Sampson et al proposed a consensus that is widely agreed upon.3
Anaphylaxis is likely when any one of the three following criteria is met:
1. Acute onset of an illness with involvement of skin and/or mucosal tissue (flushing, urticaria, angioedema) with at least one of the following:
a. Respiratory compromise (e.g. dyspnea, bronchospasm,
stridor)
b. Hypotension or associated symptoms of end-organ dysfunction (e.g. hypotonia, syncope)
2. Two or more of the following rapidly occurring symptoms following exposure to a likely allergen:
a. Involvement of the skin-mucosal tissue (generalized hives, swollen tongue)
b. Respiratory compromise (e.g. dyspnea, bronchospasm, stridor)
c. Hypotension or associated symptoms (e.g. hypotonia, syncope)
d. Persistent gastro-intestinal symptoms (e.g. abdominal
pain, vomiting)
3. Hypotension and exposure to a known allergen for the patient
a. Infants and children: low systolic blood pressure (age specific) or > 30% decrease in systolic blood pressure
b. Adults: systolic blood pressure of < 90 mmHg The syndrome can develop in minutes to hours, therefore the sedation practitioner must be vigilant and able to
recognize the development of symptoms suggestive of anaphylaxis. Monitors cannot change the outcome, therefore practitioners need to monitor what they cannot
control. We accept that different levels of sedation require different standards of monitoring, yet, any patient who receives sedation of any kind needs some monitoring
according to SASA Guidelines. Moderate sedation levels require continuous monitoring that includes pulse oximetry, heart rate, respiratory rate and pattern of breathing, and
the recording of blood pressure.4
The manifestations of anaphylaxis are seen in the cardiovascular system, upper and lower respiratory tract, gastrointestinal tract and skin. Some or all of the following
features can be present: nasal congestion, rhinorrhoea, lacrimation; generalized erythema, pruritus, urticarial, angio-oedema, bronchospasm, laryngeal oedema, nausea,
vomiting, hypotension, myocardial ischaemia and cardiac arrhythmias.5
A feeling of impending doom (angor animi) is often the first symptom to occur.
Food most commonly triggers anaphylaxis in children, and drugs in adults. Certain drugs like muscle relaxants, antibiotics and aspirin are more often the culprits.6
Local anaesthetics: Anaphylactic reactions to amide and ester type local anaesthetics are extremely rare.7
Propofol has a 1:60 000 incidence of anaphlaxis. Initially there was a higher incidence due to the cremophor used as a preservative.8
There is not an increased incidence in patients allergic to eggs.7
Antibiotics: Penicillin is the most common cause of anaphylaxis in the community and may be responsible for up to 75% of deaths due to anaphylaxis.7
Only a minority of patients who report an allergic reaction to penicillin have a documented allergy on skin testing.7
SADJ September 2016, Vol 71 no 8 p368 – p369
JA Roelofse,1
C Lapere,2
A von Backstrom3
Continuous education in sedation: Anaphylaxis management during
procedural sedation
1. James A Roelofse: MB.ChB, MMed, PhD, Dip NDBA (USA).
Professor University of the Western Cape, Visiting Professor,
University College London.
2. Cherese Lapere: MB.ChB, DipPEC, DA(SA), PDD. Sedation
Practitioner.
3. Andre von Backstrom: MB.ChB, Dip Sed. Sedation Practitioner,
Sedation Solutions, London.
Corresponding author James A Roelofse:
Private Bag X1, Tygerberg 7505. Tel: 021 937 3085,
Cell: 083 458 2427. E-mail: jar@sun.ac.za
< 369 www.sada.co.za / SADJ Vol 71 No. 8 sedation
Certain factors contribute to the severity and the fatality risk of anaphylactic reactions: poorly controlled asthma (particularly in adolescents and young adults), underlying
cardiovascular disease and extremities of ages (young children and adults above 55).9
Important chemical mediators of anaphylaxis include cytokines, preformed granule-associated substances (histamine, tryptase, chymase) and lipid derived mediators
(prostaglandins, leukotrins). These are released due to the degranulation of mast cells and basophiles.2
Histamine release is the pivotal event that activates H1 and H2 receptors.
Activation of H1 receptors causes pruritus, rhinorrhoea,
bronchospasm, flushing and tachycardia. H2 receptors
mediate increased vascular permeability and hypotension.
These chemical mediators could affect the myocardium directly.
H1 receptors mediate coronary artery vasospasm and increase
vascular permeability. H2 receptors mediate increased atrial and
ventricular contractility, increased atrial rate and coronary artery
vasodilatation. Anaphylaxis has been associated clinically with
myocardial ischemia, conduction defects, atrial and ventricular
arrhythmias and T wave abnormalities.
The treatment of anaphylaxis should begin with a rapid
assessment, maintenance of airway, breathing and
circulation and recognition of the presenting alarm
symptoms.3
Help should be called immediately and the
practitioner should initiate emergency treatment.3
Of great
importance is the discontinuation of the exposure to the
allergen (if known). When the criteria for the diagnosis
are fulfilled, adrenalin should be given without delay.3
The sedation practitioner needs to be able to identify these
clinical features in correlation with the diagnostic criteria to
prevent the delay of life-saving treatment.
A prominent risk factor for fatal anaphylaxis is the delay in the
administration of adrenaline. Early administration of adrenaline
is defined as the correct dose given within 30 minutes of
exposure to the allergen: 0,01mg/kg (0.5mg maximum dose)
administered intramuscularly (anterolateral thigh), repeated every
5-15 minutes.3,10 Intravenous dose is dependent on severity:
10μg-1mg boluses, with subsequent infusions as needed.
Further management includes patient positioning by elevating
the legs in the supine position3,  and rapid intravenous
fluids via large bore cannulas, concurrently giving high flow
of oxygen.1
H1 antagonists: e.g. Diphenhydramine/Promethazine
25-50mg given intramuscularly or slow intravenous
administration of H2 antagonists: Ranitidine 1mg/kg or cimetidine
4mg/kg. Treat bronchospasm as per usual protocol.
Should cardiac arrest occur, good quality CPR should
be initiated immediately as per current resuscitation
protocols, including intravenous adrenalin.10
Patients taking β-adrenergic antagonists may be more likely
to experience severe reactions characterized by a slow
pulse, severe hypotension and bronchospasm. Glucagon
can be given to these patients.11
The major causes of death due to anaphylaxis is listed as
asphyxia, shock, disseminated intravascular coagulation
and adrenalin overdose.
Recurrent or biphasic anaphylaxis may occur in up to 20%
of patients3, usually within 8-12 hours. Corticosteroids
should be given to prevent the incidence of recurrence,
Hydrocortisone up to 2g or Methylprednisolone as an
alternative, can be given intravenously.
The patient should be referred to an Emergency unit for
further management.
After an anaphylactic event, the patient should be referred
to an allergist for testing. Skin-prick, intradermal or
serological testing are the usual modalities used. Skin
prick testing has a high predictive value in the setting of a
history of anaphylaxis. Intradermal testing is used for local
anaesthetics, propofol and muscle relaxants. Skin testing
should be performed 4-6 weeks after an anaphylactic
reaction. Risk of triggering anaphylaxis is small (<0,1%),
but resuscitative equipment must be available.
Measures to reduce the incidence of anaphylaxis and
anaphylactic deaths include appropriate training and
counseling on the use of auto-injectors for the patient and
their families.1
Patients should also wear bracelets or warning
identification. Patients and families need to be taught to
use the adrenaline auto-injector and cautioned to keep the
adrenaline kit with them. Patients need to be able to identify
the allergen to which they are allergic and know how to avoid
it.1
All anaphylactic drug reactions should be reported.
Sedation practitioners always need to obtain a thorough
history for drug allergy.
Conclusion
Anaphylaxis is a severe, life-threatening, systemic
reaction that can occur within minutes after exposure
to an allergen. Sedation practitioners need to know the
clinical presentation as well as subtle signs and symptoms
suggestive of the diagnosis. Early adrenalin administration
is the key to the survival of patients with anaphylaxis.
References

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