Page 578 - ACCCN's Critical Care Nursing

Management of Shock 555

However, in this study, less than 1% of the population be considered when there are two or more organ systems
actually suffered an anaphylactic reaction manifesting involved. 125
with generalised multisystem allergic reaction, including Of note is the high mortality in patients with asthma and
evidence of airway involvement, rashes, GIT and cardio- those on beta-blocker or ACE inhibitor medications; 119,126
vascular dysfunction. 123
these medications may limit the effectiveness of adrena-
This allergic response is via a host mast-cell reaction line therapy. Age and preexisting lung disease are the
mediated by immunoglobulin E (IgE), and an antibody most important factors in relation to severity; older
118
produced in response to the allergen that is attached to people and those with asthma or airways disease have a
basophils (mast cells). Once sensitised to an allergen, higher risk of a life-threatening reaction. 124
subsequent exposure may lead to an anaphylactic reac-
tion in affected individuals. The mechanism is that sub- NURSING PRACTICE AND COLLABORATIVE
sequent exposure leads to mast-cell–allergen complexes CARE: INITIAL MANAGEMENT
and the release of histamine. 124 Reactions to an allergen Diagnosis of an anaphylactic reaction requires an appro-
cannot be predicted in anaphylaxis, with a subsequent priate assessment and history, including acute onset,
119
exposure leading to an amplified or lesser response. history of allergic reaction and initial measures instituted
There can be an initial reaction, which subsides with to support airway, breathing and circulation (ABC).
treatment over about 24 hours, but often described is a Removal of the causative agent (if possible) and early
second or rebound reaction up to 8–10 hours after initial treatment (within 30 minutes of exposure to an allergen)
exposure to an allergen. 118,122
results in improved outcomes. ABC measures are impor-
CLINICAL MANIFESTATIONS tant considering the rapid impact of circulating mediators
and potential decline in respiratory and cardiovascular
Exposure to an allergen causes release of histamine and function. Securing the airway is vital as most anaphylactic
other mediators, with subsequent vasodilation and related deaths are due to asphyxiation. Adrenaline is
121
increased microvascular permeability – a distributive recommended as first-line drug treatment 119,121,122,124 often
form of shock. Histamine acts, and is metabolised, rapidly as an IM injection.
while other mediators have a sustained effect. The
121
antigen–antibody reaction may directly damage vascular NURSING PRACTICE AND COLLABORATIVE
walls, while release of vasoactive mediators such as his- CARE: AIRWAY MANAGEMENT
tamine, serotonin, bradykinins and prostaglandins trigger
a systemic response, resulting in vasodilation and Early elective intubation is recommended for patients
increased capillary permeability, with widespread loss of with airway oedema, stridor, or any oropharyngeal swell-
fluid into the interstitial space and hypovolaemia. Blood ing. Patients with airway swelling and/or angiooedema
pressure and cardiac output/index may fall with a com- are at high risk for rapid deterioration and respiratory
125
pensatory rise in heart rate. Severe bronchospasm may compromise. Late presentation to hospital or delayed
also occur from mediator-induced bronchial oedema and intubation when airway swelling is present may mean
pulmonary smooth muscle contraction. Abdominal that intubation and other emergency airway procedures
9
pain is thought to be due to the inflammation of Peyer’s may be extremely difficult. Multiple attempts at intuba-
patches (clusters of lymphatic tissue containing tion increase laryngeal oedema or cause trauma to the
B-lymphocytes, located in the mucosa and submucosa of airway. Early recognition of the potentially difficult airway
the small intestine). 124 A list of signs and symptoms for allows planning for alternative airway management by
125
anaphylaxis appears in Table 20.10. Anaphylaxis should experts in difficult airways.
NURSING PRACTICE AND COLLABORATIVE
CARE: ADJUNCTIVE SUPPORT
Adjunctive drugs include H 2 -antagonists, antihistamines,
corticosteroids and other beta 2 -agonists for airway symp-
TABLE 20.10 Clinical manifestations of toms. The H 2 -antagonists are competitive antagonists of
anaphylaxis 119,122,123 histamine at the parietal cell H 2 receptor. Blocking both
H 1 and H 2 receptors is an advantage with urticaria
System Clinical manifestations present. Corticosteroids may be beneficial for persistent
Nervous Syncope, dizziness, weakness, seizures, anxiety bronchospasm, asthma and severe cutaneous reactions
Respiratory Stridor, wheeze, cough, pharyngeal/laryngeal but not in acute management. Glucagon and noradrena-
oedema, dyspnoea, bronchospasm, line may be required for patients on beta-blockers who
tachypnoea, cyanosis, use of accessory may have resistant severe hypotension and bradycar-
muscles dia. 127 Glucagon exerts positive inotropic and chrono-
Cardiovascular Tachycardia, hypotension, arrhythmias tropic effects, independently of catecholamines, while
atropine may reverse bradycardia. Vasopressin is also
Abdominal Nausea, vomiting, cramps, pain, diarrhoea 121
suggested where shock is refractory to adrenaline.
Other Flushed skin, pruritus, urticaria, angiooedema, Given that a second reaction may occur after the initial
erythema, rash, lacrimation, conjunctival allergic response, monitoring should continue for up
injection, warmth, itching 121
to 48 hours.