Download ANAPHYLAXIS

ANAPHYLAXIS
Immunological &
non-immunological
mechanisms combine
to create a clinical
presentation known
as anaphylaxis
A life-threatening histamine &
vasoactive mediated systemic event
A severe hypersensitivity reaction resulting in
cardiovascular &/or respiratory compromise
SKIN; Urticaria or generalised acute
pruritis
RESPIRATORY; airway spasm, oedema,
feeling of pharyngeal constriction
CARDIOVASCULAR; shock
GASTROINTESTINAL; cramps &
diarrhoea
Histamine actions
Relaxes vascular smooth muscle
Increased capillary permeability
Constricts bronchial smooth muscle
Life is threatened
Cardiovascular collapse
Bronchospasm
Laryngeal oedema
 Anaphylactic reactions can be observed as the development of
flush or pallor, urticaria, angioedema, hypotension, tachycardia, &
bronchospasm esp. in asthmatics.
 Reaction occurs usually within a few minutes of IV drug
administration, or longer in administrated via other routes.
 May be followed by abdo cramps, diarrhoea & abnormal
coagulation.
Causes
Stings, food, antibiotics, contrast media, thrombolytics, non-steroid antiinflammatory drugs, anaesthetic agents
FACTORS THAT INFLUENCE MORTALITY; asthma, pre-existing
hypovolaemia, heart failure, coronary artery disease predispose the
patient to increased levels of severity & potentially fatal complications.
Drugs may blunt response to adrenaline (beta blockers)
Severe anaphylaxis is an important cause of PEA – pulseless electrical
activity = cardiac arrest in presence of ECG complexes but no palpable
pulse, thought to deteriorate to asystolic arrest due to hypovolaemia &
hypoxia.
Severity
Varies from trivial erythema or urticaria
to full blown cardiovascular collapse
and asphyxia
Mortality is influenced by:
Asthma
Pre-existing hypovolaemia
Heart failure
Coronary artery disease
ECG findings in patient collapse
associated with severe
anaphylaxis
PEA; cardiac arrest in the presence of
ECG complexes but no palpable pulse
and is thought to deteriorate to
asystolic arrest due to hypovolaemia
and hypoxia
Immediate management
Remove trigger
Position supine
High flow oxygen
Management
 ADRENALINE; constricts vascular beds, reducing hypotension
& capillary leak & dilates bronchial smooth muscle.
 Most important drug in anaphylaxis management – but
remember does increase heart rate,, myocardial irritability &
inotropy (force of muscle contraction) – therefore
predisposing the myocardium to potentially serious
arrhythmias & increased myocardial oxygen requirements
predisposing to ischemia. Life threatening shock = IV admin /
IM route in majority of situations
 FLUID THERAPY; rapid fluid replacement therapy required to
replace fluid losses from circulation – isotonic saline is an
acceptable alternative to colloidal fluids
 ANTIHISTAMINES; at best second line treatment evidence
supporting use is weak and may cause further hypotension.
(block the receptor action of histamine therefore may
contribute to reducing vascular actions. 2 types of
antihistamines; H1 blockers – i.e. promethazine & H2 blockers –
i.e. ranitidine.)
 H1 blockers are most important in obtunding the
cardiovascular effects of histamine (H2 blocker may be useful
in cardiovascular collapse that responds poorly to adrenaline,
fluid & H1) H1 blocking antihistamines are rarely life saving in
severe anaphylaxis but should be routinely used in
combination with other treatments.
 CORTICOSTERIODS; slow acting- uncertain benefit in acute
phase. Administration must not delayed more life saving
therapy (adrenaline & fluids) a parenteral dose may be given
in cases of suspected anaphylaxis once initial resus and
stablisation is complete.
 Management is matched to the severity of presentation
Adrenaline - Fluid therapy
- Antihistamines
Corticosteroids
If the patient is shocked and
exhibiting signs of angioedema or
bronchospasm >>
ADRENALINE:
- 0.3-0.5ml of 1:1000 IM, repeat q5min if no improvement
Fluid:
- rapid infusion of 1000mls isotonic fluid
Management relates to severity of
symptoms
 Repeat IM adrenaline after 5 minutes if there is no improvement in
hypotension, airway swelling or bronchospasm
 IV 0.5-1ml of 1:10,000, increase dose as required
 IV adrenaline is indicated if the situation cardiac arrest
 Management relates to severity of symptoms
 Degree of cardiovascular collapse; pulse & blood pressure
 Development of swelling of upper airway; stridor & ability to articulate
 Degree of brochoconstriction; wheeze & ability to ventilate
 Fluid administration is guided by response to adrenaline and
persisting hypotension
 continued adrenaline suggests additional fluid requirements
 1-3 litres is commonly needed, if more is required consider CVP
monitoring
Additional considerations
Nebulised salbutamol 5mg
IV fluids: secure access & titrate
infusion to maintain blood pressure
Hydrocortisone 200mg IV stat
Consider nebulised adrenaline 1mg if
angioedema persists or worsens
Contact ICU if patient not responding
to interventions
Cardiac arrest
Consider giving escalating doses of IV
adrenaline if still in cardiac arrest
>5 minutes
Fluid resuscitation 2 L rapidly
Continue CPR for longer than usual
New Zealand Resuscitation Council; Whakahauora Aotearoa, August 2011