Transcript Anaphylaxisx

ANAPHYLAXIS
Approach and Management
As part of Lady Minto Hospital Emergency Rounds and
All Day Emergency Simulation Workshop
Saturday May 14, 2016
Prepared by Shane Barclay
GOALS AND OBJECTIVES
1. Review the causes and clinical presentation of anaphylaxis.
2. Review the management of acute anaphylaxis.
3. Practice clinical scenarios of anaphylaxis in the simulation lab.
DEFINITION OF ANAPHYLAXIS
- an acute, potentially life-threatening hypersensitivity reaction, involving
the release of mediators from mast cells, basophils and recruited
inflammatory cells.
Anaphylaxis is defined by a number of signs and symptoms, alone or in
combination, which occur within minutes, or up to a few hours, after
exposure to a provoking agent.
It can be mild, moderate to severe, or severe. Most cases are mild but any
anaphylaxis has the potential to become life-threatening, often within
minutes.
CAUSES OF FATAL ANAPHYLAXIS
1. Medications (most common trigger in adults)
- beta lactam antibiotics - the most common cause
- radiocontrast agents
- allergy immunotherapy
2. Foods (most common trigger in children)
- In order of frequency : peanuts, tree nuts, cow's milk and seafood
3. Insect stings (second most common trigger in adults)
- yellow jacket, honey bee, wasp, hornet, and fire ants
FATAL ANAPHYLAXIS
Analysis of fatal anaphylaxis show that in most cases of death, less the 60
minutes elapsed from allergen exposure to time of death.
With medications, symptoms appeared after an average of 5 – 10 minutes.
With insect stings, symptoms appeared after an average of 10 -15 minutes.
With foods, symptoms appeared after and average of 25 – 35 minutes.
The most common cause of death is cardiovascular and/or respiratory
arrest.
PATHOPHYSIOLOGY OF ANAPHYLAXIS
A number of mediators including histamine, nitric oxide, calcitonin generelated peptide, platelet-activating factor and others all contribute to the
cardiovascular and pulmonary features of anaphylaxis.
The end result however is a syndrome like hypovolemic shock (not
necessarily the traditional view that anaphylaxis was distributive shock
like in sepsis). There is massive fluid extravasation causing reduced
venous return and depressed myocardial function.
Up to 35 % of the intravascular volume can shift to the extravascular
space within 10 minutes during anaphylaxis. This can result in what is
known as ‘empty ventricle syndrome’.
PATHOPHYSIOLOGY OF ANAPHYLAXIS
Anaphylaxis can also be associated with cardiac ischemia and conduction
abnormalities.
Most patients will present with tachycardia, but some will be bradycardic
after this initial phase. Patients are often then hypotensive and
bradycardic.
If cardiac arrest occurs, the most common rhythm is PEA.
DIFFERENTIATING ALLERGIC
VERSUS ANAPHYLAXIC REACTION
This can be difficult and is probably the most common error in treating
anaphylaxis – ie failure to realize the patient is having an anaphylactic
reaction and NOT just an allergic reaction.
In fatal anaphylaxis, median times to cardiorespiratory arrest are 5
minutes in iatrogenic anaphylaxis, 15 minutes in stinging insect
venom-induced anaphylaxis, and 30 minutes in food-induced
anaphylaxis.
DIFFERENTIATING ALLERGIC
VERSUS ANAPHYLAXIC REACTION
Several studies of fatal anaphylaxis have shown that
the most common mistake is
not giving epinephrine early enough or not at all!
CLINICAL PRESENTATION OF
ANAPHYLAXIS
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Respiratory compromise. Wheezing, dyspnea, stridor.
Hypotension – Systolic < 90 mmHg.
Skin/mucosal involvement – hives, itch, flushing, swollen lips
/tongue/uvula, pilar erection
Persistent gastrointestinal symptoms – cramps, abdominal pain,
vomiting.
Anxiety, apprehension, sense of impending doom.
Seizures, headache.
Uterine cramping and/or bleeding.
BIPHASIC REACTION
Biphasic reaction is the recurrence of symptoms that develop after the
apparent resolution of the initial anaphylactic reaction without additional
exposure.
Can occur in up to 20% of patients
Usually occur within 10 hours of initial reaction, but have been reported to
occur up to 72 hours later.
CONCURRENT MEDICATIONS
Patient who are taking:
Beta blockers
ACEI
alpha-adrenergic blockers (eg trazadone, antipsychotics, mirtazapine)
All increase the chance of fatal anaphylaxis and can block or
interfere with treatment response (epinephrine)
MANAGEMENT
Epinephrine 0.3 – 0.5 mg IM (lateral thigh)
Is the most important treatment.
There are NO absolute contraindications to epinephrine use.
If no response to IM epinephrine start IV infusion.
Epinephrine infusion: start 1 – 5 mcg/min then titrate.
Worth mixing up push dose epinephrine if infusion is going to take
time to mix.
Use 9 cc N/S in 10 cc syringe. Add 1 cc of 1:10,000 cardiac ampule.
(in yellow boxes in crash cart)
Makes 10 mcg/ml. Give 5 – 10 mcg IV (0.5 – 1 cc IV)
MANAGEMENT
Stop or remove inciting agent
- eg. stop iv infusion of drug.
Place patient in supine position with legs elevated.
Give supplemental oxygen. Use 100% via non rebreather.
Give salbutamol via nebulizer.
IV fluid volume resuscitation. May need 1 -2 liter bolus N/S.
MANAGEMENT
If patient on beta blockers give Glucagon.
Helps reverse the bronchoconstriction effect of beta blockers.
Glucagon: 1- 5 mg IV over 5 minutes
(If given too fast can cause vomiting)
Then start infusion at 0.05 – 0.15 mg/kg/h
MANAGEMENT
Airway:
Use high flow oxygen with nebulized salbutamol
Intubate if any indication of impending airway obstruction or
angioedema.
Remember with angioedema these may be difficult intubations.
Be prepared for Cricothyrotomy.
If normotensive can use standard RSI protocol.
If hypotensive use ‘shock intubation’ protocol.
MANAGEMENT
H1 Antagonists – antihistamines (Benadryl)
These help itch and hives but do not treat upper airway
bronchoconstriction.
If given IV can worsen hypotension.
H2 Antagonists (Ranitidine)
Help with itch but also have no benefit in treating anaphylaxis.
If used give Ranitidine 50 mg IV
MANAGEMENT
Corticosteroids
- There are no clinical trials showing benefit in treatment of acute
anaphylaxis.
- Take several hours to be of any benefit.
- Rationale for using is to prevent the biphasic response in
anaphylaxis
- If used give Methylprednisolone 1-2 mg/kg daily PO.
CLINICAL SCENARIO 1
27 year old male with known peanut allergy inadvertently ate a sauce that
had peanut oil.
Within 1 minutes he developed hives, generalized flushing, feeling unwell
and sweaty.
He presents to the ER looking ill, flushed and hives on his face and neck.
BP 110/75, HR 140, Sats 98% RR 28/min
CLINICAL SCENARIO 1
What are you going to do?
CLINICAL SCENARIO 2
A 45 year old woman was started on Pen V by her dentist
earlier this morning. After the first pill she noticed some
mild flushing, feeling warm and mild rash on her trunk.
No itch.
After taking the second pill 30 minutes ago she again
noticed flushing, an itchy rash on her trunk and arms.
CLINICAL SCENARIO 2
Past history: Hypertension
Medications: HCTZ 12.5 mg od, Ramipril 5 mg od
On presentation: she looks anxious but no respiratory
distress.
She has hives on her face, neck and arms.
BP 130/65 HR 145, RR 26, O2 sats 90%
CLINICAL SCENARIO 2
What are you going to do?
CLINICAL SCENARIO 3
68 year old male was just admitted to hospital with
cellulitis and is being started on IV antibiotics.
Past history:
CAD with 2 stents
Asthma
Chronic renal insufficiency
Gout
CLINICAL SCENARIO 3
Allergies: none known
Medications:
Ramipril 5 mg od
Metoprolol 12.5 bid
ASA 81 mg od
Atorvastatin 40 mg od
Symbicort 200 bid
Salbutamol bid prn
CLINICAL SCENARIO 3
The nurse calls you to see him as he is appearing unwell.
When you come in the room he is diaphoretic, rash over
his face and upper trunk. Lips appear slightly swollen.
He looks at you ‘with fear in his eyes’.
You can hear audible wheezing as he breathes.
His IV is running (with the antibiotics).
Vitals: BP 110/40 HR 145, RR 40, O2 Sats 92%
CLINICAL SCENARIO 3
What are you going to do?