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SpongeDude

Checking airway- Allergic reaction

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OK- I know this is basic and simple but just want some feedback.

We were dispatched for a "possible" allergic reaction to food.... we get on scene and pt stated her throat flet like it was closing.... Upon examination we found her ABC's to be fine- lungs clear, Alert & oriented x3 etc etc- seems to be in fine shape-

What is the best way to assess the airway upon this complaint? Should you visually look?- outside of ling sounds- how about putting a scope right on the midline throat area?? Just looking for quick ways to assess and decide how serious....

In this case- she was totally fine and it appeared more anxiety related- but I was looking for some other ways to go about this type of assessment

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Allergic reaction(s) is caused by an histamine response. The usual urticaria (rash) and maybe angioneurotic edema (swelling of tongue, throat, upper airway) and of wheezes & stridor. The patient on top of rash may develop hives or welts (not whelps as most mis-pronounce.. which is baby puppies).

The more common allergic reaction occurs within 30 minutes after ingestion, can occur later but some studies shown it is least likely to. More common allergies are peanuts, and seafood (iodine).

I would recommend assessing the skin for the rash, see if she is itching, any welt formation ?.. Check upper airway for tongue swelling or tightness in throat or is the palate itching?.. Some people can be very anxious so it is hard to determine, but reassurance and monitoring will calm them down to be able to examine. Again, if there is not a reaction usually within the first 15 minutes chances are it might not be an reaction. The patient still needs to be monitored in case of delay response.

The usual tx. of ananphylaxis if the patient is truly developing. Dependent on your local protocol (i.e Epipen..oxygen, notify ALS , etc) ALS may administer H[sub:76cb1f67c5]2[/sub:76cb1f67c5] blockers such as Benadryl, Pepcid, Zantac, or even steroid such as Solu-Medrol, Decadron, or Kenalog.

Be safe,

R/R 911

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Allergic reaction(s) is caused by an histamine response. The usual urticaria (rash) and maybe angioneurotic edema (swelling of tongue, throat, upper airway) and of wheezes & stridor. The patient on top of rash may develop hives or welts (not whelps as most mis-pronounce.. which is baby puppies).

Be safe,

R/R 911

LMAO...sorry Rid...that was funny. Congrats....you made me laugh on what is otherwise an impossible ucky Monday morning....

xoxoxo

8 :wink:

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Well its been my experience that most people are aware they have allergies and know what they are sensitive to. When someone tells you they are having a reaction and they had experienced it before. You can believe them. I would get a quick history as to what triggered this. Then they get Epi and the Beni. (if they are not sensitive to it) asap. Don't take the time to screw around. Give it and always prepare for airway control. Yes rash and WELPS,,he,,he,, are good indicators but don't rely on that alone. A visual of the airway is fine, But don't screw around putting scope blades or anything else in the airway. If they are indeed having a reaction you could create a bigger problem with spasm. Then your ass puckers, pretty damn tight. Pass me the toilet paper along with the surgical airway kit!

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Seldomly have I seen a systemic response to an ingested allergen. Usually it's angioedema.

Assess the tongue, uvula and their voice. Do they sound hoarse or muffled? Can they swallow, breathe through their mouth and nose? Can they stick their tongue out?

Decreased lung sounds is usually a late and ominous sign. If they complain of a sensation of their throat closing and you see evidence of such, believe them.

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I wouldn't give medication unless the patient had signs & symptoms of an allergic reaction such as coughing, cramps, hives, itching, shortness of breath, tightness in the chest, swelling of the face, tongue or throat, nausea, vomiting or wheezing.

I usually give Albuterol 2.5-5.0 mg via HHN PRN, Benadryl 25-50 mg IM/IV, Tagament 300 mg IV, Solu Medrol 125 mg IV.

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There is a thread about this called 'anaphylaxsis' which details and answers your question. IF YOU HAD DONE A SEARCH YOU WOULD HAVE FOUND IT HERE::: "EPI" and its admin and "anaphalyaxsis", Please see this "thread" here:::Teaching Points::: ANAPHYLAXIS/EPI , & Teaching Points::Epinephrine , http://www.emtcity.com/phpBB2/viewtopic.php?t=3316

http://www.emtcity.com/phpBB2/viewtopic.php?t=1050

http://www.emtcity.com/phpBB2/viewtopic.php?p=68703

Hope this Helps,

ACE844

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At what point did he ask about epinephrine or anaphylaxis? Once again I made the mistake of giving you the benefit of the doubt ace, and followed your links so I could read through a million completely irrelevant post looking for his answer....

If you have such a hard-on for searching...God bless you...but you waste more bandwidth with your pics than all the repeated posts together...

Get off his back, let the folks ask their questions...

By the way if you do a search for "ace-search function" you will find it's been covered ad nauseum...

Dwayne

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At what point did he ask about epinephrine or anaphylaxis? Once again I made the mistake of giving you the benefit of the doubt ace, and followed your links so I could read through a million completely irrelevant post looking for his answer....

If you have such a hard-on for searching...God bless you...but you waste more bandwidth with your stupid pics than all the repeated posts together...

Get off his back, let the folks ask their questions...get a hobby or something...

Dwayne

"Dwayne,"

Your a smart guy, and your usually on the ball. So I'll help ya out here.. :wink: :P:lol:

Here's the original post::

OK- I know this is basic and simple but just want some feedback.

We were dispatched for a "possible" allergic reaction to food.... we get on scene and pt stated her throat flet like it was closing.... Upon examination we found her ABC's to be fine- lungs clear, Alert & oriented x3 etc etc- seems to be in fine shape-

What is the best way to assess the airway upon this complaint? Should you visually look?- outside of ling sounds- how about putting a scope right on the midline throat area?? Just looking for quick ways to assess and decide how serious....

In this case- she was totally fine and it appeared more anxiety related- but I was looking for some other ways to go about this type of assessment

The original poster asked how one may assess a pt with this syndrome..CORRECT. The answer can be found here::Teaching Points::: ANAPHYLAXIS/EPI

Anaphylaxis in its broadest sense represents a spectrum of clinical events from sneezing to shock depending on end organ sensitivity. Anaphylaxis is characterized as an explosive event resulting from release of histamine and preformed mediators causing profound end organ dysfunction (cardiac, respiratory, GI, dermatologic, neurologic).

Immediate hypersensitivity reactions to foreign proteins were first appreciated 4000 years ago, in descriptions of insect sting fatalities. Reactions to stinging insects still claim 50 lives annually. Subsequently, the use of horse serums, (tetanus, diphtheria) and penicillin focused attention on the overwhelming effect antigens in the right host could quickly elicit. These effects are varied and encompass clinical manifestations such as hypotension, cardiac arrhythmias, asthma, urticaria, angioedema, profuse diarrhea, nausea, vomiting and rhinitis. In l966 Drs. K. and T. Ishizaka identified the immunoglobulin in humans primarily responsible for these reactions, IgE. In the last 22 years, fascinating insights into the mechanism of this immunologic reaction, both in its "normal gate-keeper" function and its role in disease have been described.

V. CLINICAL MANIFESTATIONS OF ANAPHYLAXIS

A. Reactions are due to release of preformed mediators (histamine) and generation of leukotrienes, PAF. Severe reactions are marked by massive swelling of respiratory tract, constriction of bronchial smooth muscle and massive vasodilatation through mediator effect on capillary permeability.

1. Fatalities result in 3% of cases.

2.Significant upper and lower respiratory obstruction represent cause of death 70% of cases.

3. Cardiac arrhythmias and dysfunctions represent 24% of fatal cases.

4. Risk factors for fatalities include:

a. protracted course

b. Beta blockers

c. adrenal insufficiency

B. Host factors relevant to development of anaphylaxis include:

1. Antigen dose and mode of administration

2. Genetic predisposition

3. Stress/Chronic disease

4. Nutritional Status

C. Anaphylaxis may be uniphasic, biphasic or protracted.

1. Laryngeal edema occurs more frequently in protracted (57%) or biphasic (40%) cases.

2. With oral agents biphasic or prolonged reactions are more common than perceived previously.

3. Glucocorticoids do not reproducibly prevent biphasic or protracted anaphylaxis.

4. Patients with reactions need to be observed for greater than 12 hours especially if upper airway obstruction is involved.

D. Mechanisms involve IgE (atopy), IgE (non atopic) and non IgE.

1. Drugs IgE (non atopic).

a. Antibiotics - prototype is penicillin. Reactions rates are 0.7% to 8% (4-15 cases/10,000 courses of PCN) 20% of the population claim a history of PCN allergy. There is a 10% reaction rate with a negative history. Forty percent reaction rate with positive history. Skin testing is performed with the major determinant pencilloyl-poly-L-lysine (PrePen) and minor determinant (benzyl penicillin). Positive minor determinant skin test is associated with anaphylaxis. If skin tests are negative less than 3% chance of anaphylaxis. Desensitization is possible in a controlled environment. (cephalosporins, tetracyclines, nitrofurantoin, streptomycin, chloramphenicol, bacitracin, neomycin, amphotericin B).

Non IgE - vancomycin, polymyxins.

2. Foreign Proteins IgE (non atopic).

a. Insulin

b. PTH

c. ACTH

d. Asparaginase

e. Chymopapain

f. Penicillinase

g. Seminal Plasma

h. Antilymphocyte globulin

i. Hymenoptera venom

j. Fire ant venom

Insect Stings cause 50 fatalities annually. Patients with systemic reactions can receive venom specific therapy (bee, wasp, yellow jacket, hornet and fire ant). Immunotherapy is maintained at 100 micrograms per antigen for 60 months. Specific IgE and IgG titers can then help predict continued need for therapy.

3. Therapeutic agents (IgE).

a. allergic extracts

b. muscle relaxants

c. estradiol

d. hydrocortisone

e. methylprednisolone

f. protamine

g. ethylene oxide

h. thiopental

i. local anesthetics

i. Reactions are usually secondary to bisulfites or epinephrine. To document safety of a particular agent provocative skin testing can be performed.

ii. Chemically there are two groups Group I (benzoic acid ester) or Group II (amide). There is cross reactivity in Group I not in Group II. If a reaction with a Group I agent occurs (Novocaine) a Group II agent (carbocaine) can be selected.

j. vaccines

k. streptokinase

4. Foods (IgE atopic).

Fatalities usually occur in victims with prior knowledge i.e., past anaphylaxis. Usually it is a meal away from home, with alcohol, denial, reliance on p.o. antihistamines and no Epi-Pen.

a. milk

b. egg white

c. nuts

d. citrus

e. wheat

f. soybean/legumes/peanuts

g. seeds (sunflower, pumpkin)

h. grains

i. cottonseed

j. fish

k. shellfish

l. bananas

m. beets

n. corn

o. safflower

p. chamomile tea

5. Therapeutic agents (Non IgE) Reactions are secondary to anaphylatoxin production.

a. Radiocontrast media reactions occur in 20% of all procedures. Patients with prior reactions have a 17-35% change of subsequent reaction. Pretreatment with antihistamines 50mg IM l hr. before the procedure and Prednisone 50mg 13, 7 and 1 hr. before the procedure has provided effective protection in 93% of patients with prior reactions (Greenberger et.al.). Reaction is not related to iodine. Atopics allergic to shellfish have a slightly increased risk. Low osmolality contrast media has decreased reactions with increased patient comfort.

b. Transfusion reaction

c. Gamma globulin infusion

6. Modulators of Arachidonic acid metabolism. Reactions are secondary to increases in by products of lipooxygenase pathway.

a. ASA

b. Nonsteroidal anti-inflammatory agents

c. Azo dyes

d. Yellow dye #5

e. Benzoates

7. Bisulfites which are used as sanitizing agents for food containers and fermentations equipment. FDA allows in non-thiamine containing foods. Sprayed on fresh vegetables, shellfish, beer, and wine. Ingest 20-100 mg per restaurant meal. Also found in medications. Mechanism of action thought to be secondary to stimulation of afferent cholinergic reflex arc by sulfur dioxide causing massive cholinergic discharge.

8. Exercise-induced anaphylaxis characterized by cutaneous warmth, pruritus, urticaria and vascular collapse. More common in atopics. may be related to specific food ingestion prior to exercise.

9. Idiopathic anaphylaxis (73 pts. reported by Boxer et.al.) no clear reproducible triggers.

a. Usually more common in atopic females (59%)

b. Reactions are infrequent 1-6 x a year (mild) (52%)

c. Reactions are frequent 48% requiring maintenance antihistamines (H1) and prednisone. Remission has required an average of 1 yr. of prednisone therapy.

10. Progesterone allergy females who are frequently atopic demonstrate sensitivity to medroxyprogesterone documented by skin testing. Treatment involves use of androgens or oophorectomy/hysterectomy.

E. Treatment

1. Epinephrine 0.3 - 0.ml (1:1000) S.C.

2. If profound hypotension, use IV Epinephrine 2-3 ml (1:10,000), although increase incidence of arrhythmias. Repeat dose every 15-20 min. as necessary.

3. Supportive therapy with fluids, vasopressors as necessary.

4. Addition of H1 blockers, H2 blockers

5. Corticosteroids (2-4 mg/kg q 4-6 hrs.) are helpful in preventing the late phase response.

6. Glucagon 1mg bolus in patients on Beta blockers.

F. Prevention of anaphylaxis and anaphylactic death

1. Thorough drug allergy history

2. Give drug orally rather than parenterally when possible

3. Patients to wait in office 30 minutes after drug administration

4. Check all drugs for proper labelling

5. Predisposed patients to carry warning identification

6. Predisposed patients taught self-injection of epinephrine

7. When antiserum essential, use human

8. Skin test and desensitize when appropriate

Background: Anaphylaxis refers to a severe allergic reaction in which prominent dermal and systemic signs and symptoms manifest. The full-blown syndrome includes urticaria (hives) and/or angioedema with hypotension and bronchospasm. The classic form, described in 1902, involves prior sensitization to an allergen with later re-exposure, producing symptoms via an immunologic mechanism. An anaphylactoid reaction produces a very similar clinical syndrome but is not immune-mediated. Treatment for both conditions is similar, and this article uses the term anaphylaxis to refer to both conditions unless otherwise specified.

Prehospital Care:

Prehospital patients with symptoms of severe anaphylaxis should first receive standard interventions. Interventions include high-flow oxygen, cardiac monitoring, and IV access. These measures are appropriate for an asymptomatic patient who has a history of serious reaction and has been re-exposed to the inciting agent. Additional treatment depends upon the condition of the patient and the severity of the reaction. Measures beyond basic life support (BLS) are not necessary for patients with purely local reactions.

Immediately assess airway patency due to the potential for compromise secondary to edema or bronchospasm. Active airway intervention may be difficult due to laryngeal or oropharyngeal edema. In this circumstance, it may be preferable to defer intubation attempts, and instead ventilate with a bag/valve/mask apparatus while awaiting medications to take effect. In extreme circumstances, cricothyrotomy or catheter jet ventilation may be lifesaving.

Inhaled beta-agonists are used to counteract bronchospasm and should be administered to patients who are wheezing. The IV line should be of large caliber due to the potential requirement for large-volume IV fluid resuscitation. Isotonic crystalloid solutions (ie, normal saline, Ringer lactate) are preferred. A keep vein open (KVO) rate is appropriate for patients with stable vital signs and only cutaneous manifestations. If hypotension or tachycardia is present, administer a fluid bolus of 20 mg/kg for children and 1 L for adults. Further fluid therapy depends on patient response. Large volumes may be required in the profoundly hypotensive patient.

Administer epinephrine to patients with systemic manifestations of anaphylaxis. With mild cutaneous reactions, an antihistamine alone may be sufficient, thus the potential adverse effects of epinephrine can be avoided. Patients on beta-blocker medications may not respond to epinephrine. In these cases, glucagon may be useful. The Medication section describes dosage, routes of administration, and contraindications for medications discussed in this section. Antihistamines (eg, H1 blockers), such as diphenhydramine (Benadryl) are important and should be administered for all patients with anaphylaxis or generalized urticaria.

Corticosteroids are used in anaphylaxis primarily to decrease the incidence and severity of delayed or biphasic reactions. Corticosteroids may not influence the acute course of the disease; therefore, they have a lower priority than epinephrine and antihistamines.

NOW TO COVER THE PHYS. EXAM PORTION OF THE POSTERS QUESTION!!

Physical:

General

Physical examination of patients with anaphylaxis depends on affected organ systems and severity of attack. Vital signs may be normal or significantly disordered with tachypnea, tachycardia, and/or hypotension.

Place emphasis on determining the patient's respiratory and cardiovascular status.

Frank cardiovascular collapse or respiratory arrest may occur in severe cases. Anxiety is common unless hypotension or hypoxia causes obtundation. Shock may occur without prominent skin manifestations or history of exposure; therefore, anaphylaxis is part of the differential diagnosis for patients who present with shock and no obvious cause.

General appearance and vital signs vary according to severity of attack and affected organ system(s). Patients commonly are restless due to severe pruritus from urticaria. Anxiety, tremor, and a sensation of cold may result from compensatory endogenous catecholamine release. Severe air hunger may occur when the respiratory tract is involved. If hypoperfusion or hypoxia occurs, the patient may exhibit a depressed level of consciousness or may be agitated and/or combative. Tachycardia usually is present, but bradycardia may occur in very severe reactions.

Skin

The classic skin manifestation is urticaria (ie, hives). Lesions are red and raised, and they sometimes have central blanching. Intense pruritus occurs with the lesions. Lesion borders usually are irregular and sizes vary markedly. Only a few small or large lesions may become confluent, forming giant urticaria. At times, the entire dermis is involved with diffuse erythema and edema. Hives can occur anywhere on the skin.

In a local reaction, lesions occur near the site of a cutaneous exposure (eg, insect bite). The involved area is erythematous, edematous, and pruritic. If only local skin reaction (as opposed to generalized urticaria) is present, systemic manifestations (eg, respiratory distress) are less likely. Local reactions, even if severe, are not predictive of systemic anaphylaxis on re-exposure.Lesions typical of angioedema also may manifest in anaphylaxis. The lesions involve mucosal surfaces and deeper skin layers. Angioedema usually is nonpruritic and associated lesions are nonpitting. Lesions most often appear on the lips, palms, soles, and genitalia.

Pulmonary

Upper airway compromise may occur when the tongue or oropharynx is involved. When the upper airway is involved, stridor may be noted. The patient may have a hoarse or quiet voice and may lose speaking ability as the edema progresses. Complete airway obstruction is the most common cause of death in anaphylaxis.

Wheezing is common when patients have lower airway compromise due to bronchospasm or mucosal edema.

In angioedema, due to ACE inhibitors, marked edema of the tongue and lips may obstruct the airway.

To answer your question-statement "Dwayne," as you can plainly see the information IS THERE IN MY POST... Hence the reason I suggested the poster expend some ATP and use the search button in the future. Although I can't for the life of me see what part was confusing for you or wasted effort. It took ME less than 3 minutes to find. Thank you for playing, please try again.

OUT HERE,

ACE844

PS: Just for you....

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