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The document discusses anaphylaxis, a life-threatening hypersensitivity reaction that can lead to shock, emphasizing its increasing incidence despite being relatively rare. It reviews the pathophysiology, epidemiology, clinical manifestations, and management strategies for anaphylaxis and anaphylactic shock, highlighting the importance of early diagnosis and treatment with epinephrine. The document also addresses the challenges in diagnosing anaphylaxis and provides guidelines for managing acute reactions.

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4 views

The Task

The document discusses anaphylaxis, a life-threatening hypersensitivity reaction that can lead to shock, emphasizing its increasing incidence despite being relatively rare. It reviews the pathophysiology, epidemiology, clinical manifestations, and management strategies for anaphylaxis and anaphylactic shock, highlighting the importance of early diagnosis and treatment with epinephrine. The document also addresses the challenges in diagnosing anaphylaxis and provides guidelines for managing acute reactions.

Uploaded by

m.elrahl2550
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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Name : Mohammed Reda El Sayed Hessian El Rahel

ID : 202102550

Research Title : anaphylactic shock

Supervisor : prof. Usama EL Dakrory


 Abstract
Anaphylaxis is a life threatening hypersensitivity reaction that can cause shock.
Epidemiology studies show anaphylaxis and anaphylactic shock is relatively rare,
but its incidence is increasing. A review of the pathophysiology of anaphylaxis can
provide insight into clinical decisions. Diagnosing anaphylaxis can be difficult as
symptoms and history are not always obvious. Diagnostic guidelines provide an
objective tool to assess for anaphylaxis. Early intervention during anaphylaxis may
prevent development of shock. Management is focused on circulation support with
epinephrine and IV fluids, and airway maintenance. Following an acute anaphylactic reaction,
patients should be provided with a referral for follow up and educated
on avoidance of triggers and use of epinephrine autoinjectors.
Keywords: anaphylaxis, anaphylactic shock, distributive shock, management
 Introduction
In this chapter, we will learn the differences between anaphylaxis and anaphylactic shock.
Epidemiology of anaphylactic shock will be reviewed. We will also discuss
the biochemical markers and mediators most noted to triggering an anaphylactic
reaction. Lastly, we will provide a review on clinical manifestations and management
of an anaphylactic reaction in a nonclinical setting and in a clinical setting.
Throughout this chapter anaphylaxis will be defined according to the World
Allergy Organization (WAO) definition ‘a severe, life-threatening generalized or systemic
hypersensitivity reaction’ .This includes Gell-Combs Type I hypersensitivity, as well
anaphylactoid reactions that are immunologically and nonimmunological mediated.
There are few studies on anaphylactic shock, and most recommendations for
anaphylactic shock management come from major allergy organizations: WAO,
AAAA/ACAAI, and EAACI. The recommendations of these groups for management
of anaphylactic shock are presented in this chapter. Recent changes in anaphylaxis
definitions require a review of the immunologic and nonimmunologic biochemical
pathways of anaphylaxis.
Definitions
Anaphylactoid reactions
Reactions that occur via mechanisms other than IgE mediated mast cell degranulation have been
referred to as Anaphylactoid reactions. However, the WAO, AAAA/
ACAAI, and EAACI have recommended stoppage of the term . Throughout this
chapter reactions that would be included in this term will be referred to as anaphylaxis
Anaphylaxis
Anaphylaxis is typically taught as Gell-Combs classification type 1 hypersensitivity, that is IgE
mediated. However, the World Allergy Organization (WAO)
proposed a new expanded definition of anaphylaxis ‘a severe, life-threatening generalized or
systemic hypersensitivity reaction’ . This new definition of anaphylaxis now
includes reactions previously categorized as ‘anaphylactoid reactions’.
Anaphylactic shock
End manifestation of anaphylaxis, occurs when there is inadequate tissue
perfusion causing end organ damage.
Epidemiology
Studies have estimated that the incidence of anaphylaxis is between 0.05 and
2.0% of the population , although the actual incidence is not clear. Issues previously identified with
epidemiologic studies include variations in definitions, under
reporting of anaphylaxis, and unclear use of incidence and prevalence of disease .
Although the actual incidence is not clear, there have been multiple studies showing
that the incidence of anaphylaxis in the United States has increased in recent years ,
although the case fatality rate has decreased . Similar findings are reported in other
countries, with UK reporting increasing rates of anaphylaxis , but no increase
in the incidence of fatal anaphylaxis . In Australia the incidence of anaphylaxis
and fatal anaphylaxis has increased as well . One study on the incidence of
anaphylaxis with circulatory symptoms found a rate of approximately 8–9 cases per
100,000 persons per year . Severe anaphylaxis, including respiratory or circulatory
symptoms, occurs more frequently at a rate of about 1–3 per 10,000 people .
Factors that may affect the incidence of anaphylaxis include geography, seasonal
variations, age, and gender . Demographic factors associated with higher
incidence include living in northern areas of US .
Pathophysiology
Anaphylaxis is caused by massive release of biochemical mediators from mast
cell and basophils. Mast cells activation occurs mainly via antigen crosslinking of
IgE bound to FcεRI receptors on cell membranes. However, other membrane receptors can activate
mast cells as well or potentiate IgE activation . The multiple
activation pathways allow for immunologic (e.g. IgE mediated) and/or nonimmunologic activation
(e.g. drug directly interacting with receptors) (Figure 1: mechanisms of mast cell degranulation).
Some antigens may mediate effects via several
mechanisms simultaneously (e.g. vespid venom, NSAIDs, opiates). In non-IgE
mediated anaphylaxis, symptoms can occur on first exposure to an antigen as prior
exposure and sensitization is not required.
Reproduced from Spoerl et al. in agreement with publishing under terms of
the Creative Commons Attribution (CC BY) license.
Triggers and cell activation
In IgE mediated anaphylaxis, an immunogen cross links membrane bound IgE
in previously sensitized mast cell. Immunogens are typically large foreign proteins

Figure 1.
Mechanisms of mast cell degranulation. Abbreviations: RCM, radiocontrast media; TLR. Toll-like
receptor;
SCF, stem cell factor; FcεRI, high affinity IgE receptor; FcγR, IgG receptor; TCR, T-cell receptor;
NMBA,
neuromuscular blocking agent; PAF, platelet activating factor; MHC, major histocompatibility
complex.
with multiple epitope binding sites (e.g. proteins in insect venom and certain foods)
. Antigens that are too small to cross link IgE (e.g. penicillin) must first bind to
larger carrier molecules in order to elicit an immune response. Common triggers of
IgE-mediated anaphylaxis include various food, venom and medication
 Signs and Symptoms
Anaphylaxis causes a generalized systemic reaction affecting multiple organ
systems, symptoms involving the skin occur in 80–90% of cases, respiratory tract
in 70%, GI in 45%, CV in 45%, and CNS involvement in 15% . The cardiovascular and respiratory
systems are the principal shock organs in fatal anaphylaxis.
Death occurs in most often due to shock or acute respiratory distress, but DIC and
epinephrine overdose have also been cited as cause of death . Most fatal
cases of anaphylaxis due to medication or venoms are a result of shock, in food
related anaphylaxis respiratory involvement is the main cause of death although
shock is still possible .
Anaphylaxis develops rapidly with symptoms developing in minutes. Biphasic
reactions, where symptoms resolve and then reappear later occurs around 20% of
the time . A systematic review of biphasic reactions found the medium time
between resolution of initial symptoms and onset of delayed symptoms to be 11 h,
with a range of 0.2–72 h
 Management
There is a general lack of evidence basis for the treatment of anaphylaxis ,
but multiple expert guidelines highlight the chief treatment as epinephrine, oxygen,
and fluids.
 Conclusions
In my opinion, Anaphylaxis is a rapidly acting life-threatening hypersensitivity reaction.
Diagnosis of anaphylaxis can be difficult, and early recognition and treatment is
essential to prevent development of shock. Shock is more common in cases due to
medication compared to food, although shock can occur. The primary treatment
in anaphylactic shock is epinephrine, fluids, and oxygen. Additional medications
including antihistamines, steroids, and inhaled beta-agonist should be used as
needed. In patients who do not respond to epinephrine, other vasopressors or
mechanical support can be used.
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