GROUP 4

1. Nal l athambi ,
Ai swarya
2. Nagaraj an,
Venkateshwari
3. Narayanaswamy,
Ni thya
4. Nal l agatl a,
Susmi tha
5. Narra, Vi ndhya
Rani

A
N
A
P
H
Y
L
A
X
I
S


1. WHAT ARE THE SALIENT FEATURES OF
THE CASE?


Age 42 y. o
Stung on the forearm whi le worki ng i n the garden.
Local i sed swell ing.
Wi thin mi nutes, she experienced fl ushing, sweating fol l owed
by shortness of breath and dyspnea.


Fol l owed by confusi on and respi ratory di stress.

The physical presentation of respi ratory di stress i s generally
referred to as l abored breathing, whi le the sensation of
respiratory di stress i s cal led shortness of breath or dyspnea.
E.R



T = 37. 2
P = 120 beats per mi n( tachykardi a)
RR = 39 breaths per mi n( tachypnea)
BP = 69/45 (Severe hypotensi on)

VITAL SIGNS
Parameter Normal Range
Pulse 60 100 beats per min
Blood pressure (systolic) 90 140mmHg
Blood pressure (diastolic) 60 90mmHg
Respiratory rate 12 20breaths per min
NORMAL VITAL SIGNS


Generalised urti caria - Urti cari a refers to a group of di sorders
af fecting adul ts and chi l dren, i n whi ch red patches and weals
occur i n the ski n.
A weal i s a swel ling of the surface ski n. The name urti caria i s
deri ved from the common European sti ngi ng nettl e ' Urti ca
di oi ca' .
URTICARIA



The ski n swel ling seen i n urti caria i s due to the rel ease of
chemicals such as hi stamine from mast cel ls and basophils
i n the ski n, whi ch causes smal l bl ood vessels to l eak.
The weals can be a few mi l limetres or several centi metres i n
di ameter, col oured whi te or red, of ten surrounded by a red
fl are, and frequently i tchy.
Each weal may l ast a few mi nutes or several hours, and may
change shape. Weals may be round, or form ri ngs, a map-
l i ke pattern or gi ant patches.
The surface weals may be accompanied by deeper swel ling
of eyelids, l i ps, hands and el sewhere.
URTICARIA AND ANGIOEDEMA


The pati ent was noted to have wheezing.
And she had encountered i nsect sti ngs i n the past wi thout
reaction on several occasi ons.
OTHER SYMPTOMS

2. WHAT ARE YOUR DIFFERENTIALS?
Tachycardia
Damage to heart ti ssues from heart di sease
Abnormal el ectrical pathways i n the heart present at bi rth
(congenital)
Di sease or congeni tal abnormality of the heart
Anemia
Exercise
Sudden stress, such as fri ght
Hi gh bl ood pressure
Anaphylactic shock
DIFFERENTIAL FOR THE VITAL SIGNS


In anaphylaxis, the pati ent experiences tachykardia as the
heart pumps faster to compensate for the drop i n BP
Severe hypotension
mainly caused by
Bl ood l oss
Severe i nfection ( septicemia)
Severe al l ergic reaction (anaphylaxis)
Lack of nutri ents i n di et


In thi s case, the i nsect bi te wi l l tri gger the rel ease of
hi stamine i n the body cel l s whi ch causes wi despread
di l atation of the bl ood vessels whi ch accounts for the drop i n
BP.



DIFFERENTIAL DIAGNOSIS OF
ANAPHYLAXIS

V

Vasodepressor (vasovagal) reaction (probably the most
common masquerader)
Gl obus hystericus(a l ump i n one s throat)
Hereditary angi oedema
Other forms of shock ( i e, hypovolemic, cardiogeni c, septi c)
Fl ushing syndrome, i ncl uding red man syndrome
(vancomycin), pancreati c pol ypeptide tumors,
postmenopausal pati ent, ethanol - induced, autonomic
epi lepsy


Monosodi um gl utamate poi soni ng
Capi llary l eak syndrome
Pul monary embolism
Myocardial dysfunction
Foreign body aspiration (young chi l dren, especial ly)
Poi soni ng, acute
Neurologic (stroke, sei zure)

3. WHAT IS YOUR FINAL DIAGNOSIS?
SUPPORT YOUR DIAGNOSIS.


The fi nal di agnosis i s that the pati ent i s suf fering from
Anaphylaxis.
The cl i ni cal di agnosis of anaphylaxis i s based on probability
and pattern recognition.
Anaphylaxis i s consi dered l i kely to be present i f any 1 of the
3 fol l owing cl i ni cal cri teria i s sati sfi ed wi thin mi nutes to
hours:

1. Acute symptoms involving skin, mucosal surface, or both,
as well as at least one of the following: respiratory
compromise, hypotension, or end-organ dysfunction.



2. Two or more of the fol l owing occur rapi dly af ter
exposure to a l i kely al l ergen: hypotension, respi ratory
compromise, persi stent gastroi ntestinal symptoms, or
i nvol vement of ski n or mucosal surface.

3. Hypotension develops af ter exposure to an al l ergen
known to cause symptoms for that pati ent: age- specific l ow
bl ood pressure or decl ine of systol i c bl ood pressure of more
than 30% compared to basel ine.


However, anaphylaxis occurs as part of a cl i ni cal conti nuum
that can begin wi th rel atively mi l d features and rapi dly
progress to l i fe- endangering respiratory or cardi ovascular
mani festations.

Del aying the di agnosis unti l mul tiorgan mani festations of
anaphylaxis are present i s ri sky because the severity of a
reaction i s di f fi cul t or i mpossible to predict at the ti me of
symptom onset.
4. WHAT LAB TESTS CAN BE
REQUESTED?


Pl asma hi stamine l evels ri se wi thin 10 mi nutes of onset
but fal l again wi thin 30 mi nutes.
Uri nary hi stamine l evels are generally not dependabl e,
as thi s test can be af fected by di et and by bacteria i n
the uri ne.
PLASMA HISTAMINE LEVELS


Tryptase i s a trypsi nlike proteinase that i s most abundant i n
human mast cel l s and basophils.
Serum mature tryptase (previousl y cal l ed beta- tryptase) l evels
peak 60- 90 mi nutes af ter the start of an epi sode and may
persist for as l ong as 5 hours.
Serum l evels are normal l y l ess than 11. 5 ng/mL. El evated
l evels of serum tryptase occur i n both anaphyl actic and
anaphylactoid reactions.
SERUM TRYPTASE LEVEL
If the pati ent s hi story suggests an i nsect sti ng, al l ergen-
specific ski n testi ng to Hymenoptera venoms shoul d be
performed.
If those tests remain negative af ter 6 weeks i n a pati ent
wi th a seri ous reaction, then further testing can i ncl ude i n
vi tro I gE tests.
SKIN TESTING AND INVITRO IGE TESTING


Ski n testing and i n vi tro I gE testi ng shoul d be performed 4- 6
weeks fol l owing the epi sode of anaphylaxi s to i mprove the
sensi tivity of the di agnosti c test.
Ski n testing for i mported fi re ant hypersensiti vity shoul d be
performed usi ng whol e- body extracts.
SKIN TESTING AND IN VITRO IG-E
TESTING

Pati ents abi lity to i dentify the type of fl yi ng i nsect i s
unrel iable ( eg, many confuse yel low j ackets and bees),
generally mandating testi ng for al l fl yi ng Hymenoptera.

However, exceptions to thi s mandate can be made for pati ents
whose sti ngs were accompanied by steri le pustule formati on
wi thin 24 hours (pathognomoni c for fi re ant sti ng) or for
whom an i mpaled sti nger and abdomi nal remnant were found
at the sti ng si te (the honeybee evi scerates i tself as i t sti ngs)
EXPLAIN THE PATHOPHYSIOLOGY OF THE
IMMUNOLOGICAL PROCESS
WHAT IS ANAPHYLAXIS?

Ana (wi thout), phylaxis (protection).
Acute mul ti - systemic al l ergic reaction i nvol vi ng the ski n,
ai rway, vascular system, and GI.
The result of a re- exposure to an anti gen that el i cits an I gE
mediated response
Usually caused by a common envi ronmental protei n that i s not
i ntri nsi cally harmful
Of ten caused by medi cations, foods, and i nsect sti ngs
It i s a Type I hypersensitivity

HYPERSENSITIVITY REACTION

Inj urious, or pathologi c, i mmune reactions are cal l ed
hypersensitivity reactions.
Hypersensitivity reactions may occur i n two si tuations .
Fi rst, responses to forei gn anti gens may be dysregulated or
uncontrol l ed, resul ting i n ti ssue i nj ury.
Second, the i mmune responses may be di rected against sel f
anti gens, as a result of the fai l ure of sel f - tolerance
(autoimmunity).
TYPES OF HYPER SENSITIVITY
REACTIONS
Mast cell
release
histamine
and other
mediators
Immediate
hypersensitivity
Antibodies
directed
against cell
or tissue
antigens
Antibody-
mediated
Antibody-
antigen
complex
deposit in
blood vessels
immune complex
diseases
Reactions
of T
lymphocytes
T cell-mediated
diseases
ETIOLOGY
34%
37%
20%
7%
2%
Causes of anaphylaxis in a study of 266 patients (Data from
Kemp et al)
Food
Idiopathic
Drugs
Exercise
Latex, hormons,
insect bites
WHAT IS HAPPENING?

Occurs af ter reexposure to an anti gen to whi ch that person
has produced a specific I gE anti body.
Ini ti al exposure sensi tizes mast cel l s.
Anti gen specific I gE mol ecules attach to hi gh af fi nity Fc
receptors on the mast cel l surface.
On re- exposure Cross l i nki ng of I gE mol ecules on surface
causes i ntracel lular si gnaling pathway
Inflammatory mediators are released upon degranulation
PATHOPHYSIOLOGY
Fi rst exposure
Acti vation of TH2 cel l Sti mul ate I gE swi tchi ng
Allergen
TH2 Cell
B Cell
PATHOPHYSIOLOGY
Fi rst exposure
IgE production
IgE secreting B cell
IgE
PATHOPHYSIOLOGY
Fi rst exposure
IgE bi nd to mast cel l


Mast cell
FcRI


IgE
PATHOPHYSIOLOGY
Second exposure
Recogni tion
Allergen


Mast cell
FcRI


IgE
PATHOPHYSIOLOGY
Second exposure
Acti vation of mast cel l to rel ease hi stami ne and other
mediators
Allergen
Mediators


Mast cell
FcRI


IgE
Pathologic features of anaphylaxis
Laryngeal edema
Pulmonary hyperinflation
Myocardial edema
Visceral congestion or
hemorrhage
Eosinophilic infiltration
Elevated tryptase levels
Death from cardiovascular
collapse or respiratory
obstruction
MEDIATORS INVOLVED
Incl ude hi stamine, proteases, chemotactic factors,
l eukotri enes, prostaglandin D, and cytoki nes
Pri mary: rel eased before degranul ation
Interleukin 4 used by T cells induces B cell maturation
IL-3 and IL-5 released by T and mast cells are chemo attractants for
eosinophils
Secondary: come from granules

PATHOPHYSIOLOGY
Mediators
Vascoactive aminase &
lipid
Immediate
hypersensitivity reaction
(minutes)
Cytokines
Late phase reaction (6-
24 hours)
HISTAMINE
Synthesized and stored i n granules
The pri mary mediator i n the granules
Many of the si gns and symptoms of anaphylaxis are
attri butable to bi ndi ng of hi stamine to i ts receptors
3 receptors
H1
H2
H3

Binding to H
1
receptors mediates pruritis, rhinorrhea, tachycardia,
and bronchospasm.
On the other hand, both H
1
and H
2
receptors participate in producing
headache, flushing, and hypotension.


TISSUE EFFECTS OF HISTAMINE
Cardiovascular
Decreased blood pressure
Increased heart rate
Edema (separation of endothelial cells & increased permeability)
Respiratory
broncho constriction
Gastroi ntestinal
Smooth muscle contraction and diarrhea
Ski n
Urticaria

Effects of histamine on airways
Histamine
Bronchoconstriction by stimulation of H1 receptors on smooth muscles.
Mucosal edema from increased microvascular permeability (H1) leading to
transudation of fluid and macromolecules through wide intercellular gaps (> 12
nm).
Direct stimulation of vagal (cholinergic) nerves can induce airway smoothmuscle
contraction
Stimulation of H1 receptors increases mucus secretions, and
stimulation of H2 receptors increases mucus viscosity.



Effects of histamine on the heart
H1 receptors mediate coronary artery vasoconstriction and
increased vascular permeability.

H2 receptors mediate atrial and ventricular contractile forces,
atrial rate, and coronary artery vasodilation.
Decreased diastolic pressure and increased pulse pressure
Histamine
H1 receptor on
endothelial cell
L-arginine
Nitric oxide
Decreases venous return
OTHER MEDIATORS
Metabolites of arachadoni c aci d, i ncl uding prostagl andins,
pri nci pally prostaglandi n D
2
(PGD
2
) and l eukotrienes, pri nci pally
l eukotri ene C
4
(LTC
4
). PGD
2
medi ates bronchospasm and
vascular di l atation, pri nci ple mani festations of anaphylaxis.
LTC
4
i s converted i nto LTD
4
and LTE
4
, mediators of hypotension,
bronchospasm, and mucous secretion duri ng anaphylaxis i n
addition to acti ng as chemotactic si gnals for eosi nophils and
neutrophils. Other pathways acti ve duri ng anaphylaxis are the
compl ement system, the kal likrein- kini n system, the cl otti ng
cascade, and the fi brinol ytic system
ANAPHYLACTIC REACTION (SUMMARY)
Phil Lieberman: Anaphylaxis,a cliicians manual
Mast Cell
Mast cell granules
Allergen
IgE antibody
Immediate reaction
Wheeze
Urticaria
Hypotension
Abdominal cramping


Late-phase reaction
6. DIFFERENTIATE ANAPHYLACTIC FROM
ANAPHYLACTOID REACTION
Specifically, the condition anaphylaxis requires the
patient to be sensitized, and their reaction mediated
through immunoglobin E (IgE) antibodies.

An anaphylactoid reaction doesnt need the presence of
IgE antibodies for a hypersensitivity reaction to occur.

Substances initiating the anaphylactoid reaction, such
as radiopaque contrast media, nonsteroidal anti-
inflammatory drugs (NSAIDs) and aspirin cause a direct
breakdown of the mast cell and basophil membranes.
An anaphylactic reaction occurs only after the patient has
been previously exposed at least once to the antigen and is
sensitized.

An anaphylactoid reaction can occur following a single, first-
time exposure to certain agents in nonsensitized patients.

Because anaphylactic and anaphylactoid reactions produce
the same clinical manifestations and are treated exactly
the same way, we use the term anaphylaxis to refer to both
conditions.
7. STRUCTURE AND FUNCTION OF
IMMUNOGLOBULIN INVOLVED
STRUCTURAL FEATURES OF IGE
It is a monomer and its structure is very similar to
IG M except the fact that it contains an extra
constant domain that replaces the hinge.
There are two cysteine residues per CE2 domain.
They are located within the carboxyl terminal close to
one another which are linked by disulfide bond to the
other heavy chain.
Tailpiece is absent.

FUNCTION OF IGE
The major function of Ig E is its ability to bind Fc
receptors specific for Fc region in IgE. It is of two
types.

1. Tight binding receptors
-mast cells and basophils

2. Weaker binding receptor
-lymphocytes
-monocytes
-macrophages
-eosinophils and platelets


This binding stimulates degranulation of cells
releasing chemicals. So this Ig is found to be
involved in hypersensitivity allergic reactions.
Stimulates eosinophils to secrete enzymes and
protects against worm infections.
Main host defense against helminthic infections.

8. ENUMERATE THE MOST COMMON
TRIGGERS OF THE IMMUNOLOGICAL
PROCESS
Bacteria
Vi ruses
Parasi tes
Fungi
Non- pathogens:
Food: Many foods can tri gger Anaphylaxis: This may occur upon
the fi rst Known i ngestion.
Common tri ggeri ng foods vary around the worl d.
In westren cul tures, ingestion of exposure to
peanuts, wheat, nuts, certain types of seafood l i ke
shel lfish, milk and eggs are the most prevalent causes.

Bl ood typi ng mi smatched
Bl ood type postreactions
Chemicals
Pol l ens
Drugs: - the most common are l actam anti biotics (such as
peni cillin) fol l owed by aspi rin and NSAIDS. Other anti biotics
are i mpl icated l ess frequently and the reactions to NSAIDS
are agent specific meani ng that i f one i s al l ergic to one
NSAIDS they can typi cally tol erate a di f ferent one.
Other rel atively common causes i ncl ude:
Chemotherapy
Vacci nes
Protami ne
Herbal preparati ons.
Some medications ( vancomycin, morphine , x- ray contrast
among others) cause anaphylaxis by tri ggering mast cel l
degranulation.
Sti ngs
Bee Venom


9. EXPLAIN THE CLINICAL PRESENTATION
OF THE PATIENT
CLINICAL PRESENTATIONS

1. Localized swelling
2. Flushing
3. Sweating
4. Shortness of breath and dyspnea
5. Urticaria and wheezing.
T 37.2:- Normal
P 120:- Tachycardia
R 39:-Tachypnea
BP 69/45:- Hypotension.


HISTAMINE


Histamine is an organic nitrogen compound
involved in local immune responses as well as
regulating physiological function in the gut and
acting as a neurotransmitter.

Histamine triggers the inflammatory response.
PATHOPHYSIOLOGY OF ANAPHYLAXIS
Allergen crosses an epithelial and/or endothelial barrier
Access to the reactive, sensitized cells
mast cells, basophils
Release of cellular mediators leads to end-organ response in the skin,
respiratory tract , cardiovascular system , gastrointestinal tract, nervous
system.
Histamine
H1 receptor
Pruritus
Rhinorrhea
Tachycardia
Bronchospasm
H1,H2 receptors
Headache
Flushing
Hypotension
H3 receptor
Left ventricular
function
Effects of histamine on airways
Histamine
Bronchoconstriction by stimulation of H1 receptors on smooth muscles.
Mucosal edema from increased microvascular permeability (H1) leading to
transudation of fluid and macromolecules through wide intercellular gaps (> 12
nm).
Direct stimulation of vagal (cholinergic) nerves can induce airway smooth muscle
contraction
Stimulation of H1 receptors increases mucus secretions, and
stimulation of H2 receptors increases mucus viscosity.
Effects of histamine on the heart
H1 receptors mediate coronary artery vasoconstriction and increased
vascular permeability.

H2 receptors mediate atrial and ventricular contractile forces, atrial
rate, and coronary artery vasodilation.
Decreased diastolic pressure and increased pulse pressure
Histamine
H1 receptor on
endothelial cell
L-arginine
Nitric oxide
Decreases venous return
10. DISCUSS THE INITIAL TREATMENT
ALGORITHM OF THIS MEDICAL
EMERGENCY
ANAPHYLACTIC EMERGENCY

Anaphylaxis Treatment & Management.

If you are at ri sk of anaphylaxis, carry auto- i nj ectable
epi nephrine (adrenaline). Thi s i s a si ngl e dose of medication
that i s i nj ected i nto the thi gh duri ng an anaphylactic
emergency.

MILD TO MODERATE ALLERGIC REACTION

In some cases, anaphylaxis i s preceded by si gns of a mi l d to
moderate al l ergic reaction:

Swel ling of face, l i ps and eyes
Hi ves or wel ts on the ski n
Ti ngling mouth
Stomach pai n, vomi ti ng (these are si gns of a mi l d to moderate
al l ergic reaction to most al l ergens, however, i n i nsect al l ergy
these are si gns of anaphylaxis).
ACTION

For i nsect al l ergy, fl i ck out the sti ng i f i t can be seen (but do
not remove ti cks)
Stay wi th person and cal l for hel p.
Gi ve medi cations i f prescribed (whilst antihistamines may be
used to treat mild to moderate allergic reactions, if these
progress to anaphylaxis then adrenaline is the only suitable
medication)
Locate adrenaline autoinjector i f avai lable.
Contact parent/guardian or other emergency contact.


ANAPHYLAXIS (SEVERE ALLERGIC REACTION)

Continue to watch for any one of the fol lowing si gns of
anaphylaxis (severe al l ergic reaction):

Di f fi cult/noi sy breathi ng
Swel ling of tongue
Swel ling/tightness i n throat
Di f fi culty tal king and/or hoarse voi ce
Wheeze or persistent cough
Persi stent di zziness or col l apse
Pal e and fl oppy (i n young chi l dren)

ACTION
Lay person fl at - i f breathing i s di f fi cult, al l ow to si t - do not
al l ow them to stand or wal k

Gi ve the adrenaline autoinjector i f avai lable (i nstructi ons are
i ncl uded i n the ASCIA Acti on Pl an for Anaphylaxis, stored wi th
the adrenaline autoi njector)

Further adrenaline doses may be gi ven (when an additional
adrenaline autoi njector i s avai lable), i f there i s no response
af ter 5 mi nutes.
If i n doubt, gi ve the adrenaline autoi njector.





I f uncertain whether i t i s asthma or anaphylaxis, gi ve
adrenaline autoinjector FIRST, then asthma rel iever.
Adrenaline i s l i fe saving and must be used promptl y.
Wi thhol ding or delaying the gi ving of adrenaline can
result i n deterioration and death . Thi s i s why gi vi ng the
adrenaline autoi njector i s the fi rst i nstruction on the
Acti on Pl an for Anaphylaxis. If cardiopulmonary
resusci tation (CPR) i s gi ven before thi s step there i s a ri sk
that adrenaline i s del ayed or not gi ven.
I n the ambulance oxygen wi l l usually be admini stered to
the pati ent by paramedics.
Medical observation of the pati ent i n hospi tal for at l east
4 hours i s recommended af ter anaphylaxis.
An epi nephrine autoi nj ector i s a medi cal device used to
del iver a measured dose (or doses) of epi nephrine (al so
known as adrenaline) usi ng autoi njector technol ogy, most
frequently for the treatment of anaphylaxi s.

Trade names for thi s devi ce i ncl ude Epi Pen, Emerade,
Twi nj ect, Adrenacl ick, Anapen, Jext, Al l erj ect, and Auvi - Q.
ADRENALINE AUTOINJECTOR
IN OUR CASE:
Mi l d symptoms such as pruritus and urti caria can be control l ed
by administration of 0. 3 to 0. 5 mL of 1: 1000 (1 mg/mL)
epi nephrine SC or IM, wi th repeated doses as requi red at 5- to
20- mi n i nterval s for a severe reaction.

If the anti genic materi al was i nj ected i nto an extremity, the rate
of absorption may be reduced by prompt applicati on of a
tourni quet proxi mal to the reaction si te admi nistration of 0. 2 mL
of 1: 1000 epi nephrine i nto the si te, and removal wi thout
compression of an i nsect sti nger, i f present.

An IV i nfusi on shoul d be i ni ti ated to provi de a route for
admi nistrati on of 2. 5 mL epi nephri ne, di l uted1: 10, 000, at 5- to
10- mi n i ntervals,
11. WHAT ADJUNCT MEDICATIONS CAN
YOU GIVE TO TREAT?
11.ADJUNCT TREATMENT

Epi nephrine i s the most ef fective i mmediate treatment for
anaphylaxis.

It rapi dly reverses the uncomfortable fl ushing and i tchi ng as
wel l as the more seri ous probl ems wi th breathing and
dangerous drop i n bl ood pressure that accompani es most
anaphylactic reactions.

More i mportantly, i f gi ven i n ti me, epi nephrine can reverse
the l i fe- threateni ng symptoms of anaphyl actic shock. .




If you are al l ergic to i nsect sti ngs or any of the foods that
cause anaphylaxis, or i f you ever have had an anaphylactic
reaction, you shoul d contact your physician about provi di ng an
epi nephrine i nj ection ki t. ( Epi - Pen i s one common brand
name. )




Vol ume expanders such as normal sal i ne, and vasopressor
agents such as dopamine can be gi ven for hypotension.

Repl acement of i ntravascular vol ume due to postcapillary
venular l eakage may requi re several l i ters of sal i ne.

Epi nephrine provi des both - and - adrenergi c ef fects,
resulting i n vasoconstriction, bronchial smooth- muscle
rel axation, and attenuation of enhanced venular
permeabili ty.

When epi nephrine fai l s to control the anaphylactic
reaction, hypoxia due to ai rway obstruction or rel ated to a
cardi ac arrhythmi a, or both, must be consi dered.

OXYGEN THERAPY FOR RESPIRATORY
DISTRESS

Oxygen al one vi a a nasal catheter or wi th nebulized al buterol
may be hel pful , but ei ther endotracheal i ntubation or a
tracheostomy i s mandatory for oxygen del ivery i f progressive
hypoxia develops.

Vi cti m of anaphylaxis stops breathing, perform
cardi opulmonary resuscitation (CPR) i mmediatel y. Conti nue
CPR unti l the person begins breathi ng again or emergency
medical personnel take over.






I f wheezing i s caused by asthma, your doctor may
recommend some or al l of the fol l owing to reduce
i nfl ammati on and open the ai rways:

A fast- acting bronchodilator i nhal er - - al buterol (Proventil
HFA, Ventol in HFA), l evalbuterol (Xopenex ) - - to di l ate
constri cted ai rways when you have respi ratory symptoms

An i nhaled corti costeroi d - - mometasone (Asmanex),
ci cl esonide (Al vesco), beclomethasone (Qvar), fl uni sol ide
(Aerospan), fl uti casone ( Fl ovent), budesonide ( Pul micort)



A l ong- acti ng bronchodilator/corticosteroid combi nation - -
fl uti casone/sal meterol (Advair), budesoni de/formoterol
(Symbicort)

An asthma control l er pi l l to reduce ai rway i nfl ammation - -
zafi rlukast (Accol ate), montel ukast (Si ngulai r)

A non- sedati ng anti histamine pi l l - - l oratadine (Cl aritin,
Al avert), fexofenadine (Al l egra), ceti rizine ( Zyrtec) or a
prescription nasal spray - - fl uticasone propi onate ( Fl onase),
tri amci nolone acetoni de (Nasacort AQ), mometasone furoate
(Nasonex) - - i f you have nasal al l ergies


ANTI- HISTAMINE



Anci ll ary agents such as the anti histamine di phenhydramine,
50100 mg IM or IV, and ami nophylline, 0. 250. 5 g IV, are
appropriate for urti caria- angioedema and bronchospasm,
respectively.

STEROIDS

Intravenous gl ucocorticoids, 0. 51 mg/kg of medrol , are not
ef fective for the acute event but may al l eviate l ater
recurrence of bronchospasm, hypotension, or urti caria. Due to
thei r del ayed ef fect, corti costeroi ds are not fi rst - l i ne
treatments.
Steroi d drugs (such as prednisone or methyl predni solone)
H
2
- bl ocking anti histamines theoretically are attracti ve agents
for dermal and gastrointestinal (GI) mani festations, but
evi dence supporting thei r cl i ni cal ef fectiveness i s l ess than
that for H
1
- bl ocki ng agents. Some evi dence suggests that
combi ning H
1
and H
2
bl ockers may be more ef fective than
H
1
bl ockers al one.
Gl ucagon may be useful i n treati ng refractory cardiovascular
ef fects i n pati ents taki ng beta- blockers.


12. ADVICE FOR LONG TERM CARE
ADVICE FOR LONG TERM CARE:


Certain medicines, such as beta- blockers (of ten gi ven for hi gh
bl ood pressure) and angi otensin- converting enzyme (ACE)
i nhi bitors (of ten gi ven for heart di sease), may hi nder the
successful treatment of an anaphylactic reaction.
So they both shoul d be avoi ded.
DO NOT


Do NOT assume that any al l ergy shots the person has al ready
received wi l l provi de compl ete protection.
Do NOT pl ace a pi l low under the person' s head i f he or she i s
havi ng troubl e breathing. Thi s can bl ock the ai rways.
Do NOT gi ve the person anythi ng by mouth i f the person i s
havi ng troubl e breathing.

A di f ferent form of protection i nvol ves the development of
bl ocking anti body of the IgG cl ass, whi ch protects against
Hymenoptera venominduced anaphylaxi s by i nteracting wi th
anti gen so that l ess reaches the sensi tized ti ssue mast cel l s.

Specific i nterventions to reduce or prevent anaphylaxis
recurrences from some tri ggers (examples i ncl ude venom
i mmunotherapy for those wi th anaphyl axis from sti nging
i nsects such as bees, yel low j ackets, wasps, and hornets, and
desensitization for those wi th anaphylaxis from some
medications)