Anaphylactic Reaction To Diphtheria–Tetanus Vaccine

Anaphylactic Reaction To Diphtheria–Tetanus Vaccine

The New Journal of Medicine 2008;25: 186-188
Case report
Anaphylactic Reaction To Diphtheria–Tetanus
Vaccine in A Young Woman
Behçet AL ¹, Cuma YILDIRIM
1
¹ Gaziantep University Faculty of Medicine, Department of Emergency Medicine, GAZİANTEP
ABSTRACT
Anaphylaxis is a severe systemic hypersensitivity
reaction characterized by multisystem involvement,
which may include hypotension or airway compromise, it
is potentially life-threatening. The present study
describes the occurrence of an anaphylactic reaction
after the administration of dT (diphtheria-tetanus)
vaccine in a twenty-four-years old woman. As it is rarely
reported in literatures we treated this anaphylactic
reaction with corticosteroid, and antihistamine without
using epinephrine.
Key Words: Anaphylaxis, bronchospasm, corticosteroid,
diphtheria toxoid, tetanus toxoid
INTRODUCTION
Adverse reactions to vaccines are common and
those of an immunological nature, such as
anaphylaxis and Arthus type reactions, are of
more concern. But data are infrequently reported.
The mechanisms proposed are the production of
specific IgE antibodies to any of the vaccine
components and the formation of immune
complexes between IgG antibodies and the
vaccine antigens1,2. IgE mediated anaphylactic
and local reactions have been observed after
immunisation with tetanus (Ttx) and diphtheria
toxoids (Dtx) notwithstanding these are showing a
very low frequency in the whole population3-6.
Since vaccines are composed of several
constituents, the identification of the responsible
allergens or haptens requires a detailed analysis
of all the vaccine components. Components and
contaminants of toxoid vaccines, such as gelatine
or peptones and preservatives such as thimerosal,
have been reported as causal agents in these type
of reactions7-9.
The present report describes the occurrence of an
anaphylactic reaction immediately after a dT
booster dose in a woman.
CASE
A twenty-four year-old woman suffered a severe
adverse reaction after the second intra-muscular
dose of a dT vaccine that performed to the right
deltoid muscle. Ten minutes after administration,
the patient developed a large local inflammatory
response at the injection site, followed by a
186
generalized systemic reaction with erythema,
pruritus, urticaria, palpebral edema, discomfort
and
nausea.
About
45
minutes
after
administration, she had shortness of breath. We
took this information from a witness who was a
health official and lived in patient’s village. Before
administration of vaccine she was in good health,
she did not suffer from any medical condition at
that time and she did not received any
concomitant medication. The patient did not suffer
from the first dose of dT vaccine that performed
by the same health team. Two hours after the
advers reaction she was brought to our
emergency department (ED). At admission time
she had anxiety, tremor, minimal cyanosis on lips,
shortness of breath, a sense of fullness in the
throat, a sensation of chest tightness, respiratory
distress, lightheadedness, and decreased level of
consciousness. The clinical signs of systemic
allergic reactions included cutaneous flushing,
diffuse urticaria, angioedema, colicy pain in
abdomen, nausea, vomiting, bronchospasm, wheezing,
rhinorrhea, conjunctivitis and hypotension. Blood
pressure was 90/55 mmHg, pulse 124/min,
respiratory rate 17/min, temperature 37ºC and
SO2 was 90%. Complete blood count was normal
limits. In our management we started with the
ABC (airway, breathing, circulation) of resuscitation.
Vital signs, intravenous access, oxygen, cardiac
monitoring, and pulse oximetry measurements
were continuosly monitored. Methylprednisolone
125 mg IV, antihistamine-2 (H2) blockers 100 mg
(ranitidine) IV, oxygen 4 L/min with mask, 30
B. Al and C. Yıldırım
ml/kg/h 0.9 g NaCL, bronchodilator (continuous
nebulized salbutamol sulfate) 5 mg was applied
immediatelty. The systemic reaction improved
20–30 min after treatment with corticosteroid and
anti-histamines, but the palpebral and local
oedema subsided three days later. The patient
was observed for 12 hours in ED. All of the
symptoms were improved except palpebral and
local oedema. Hydroxyzine HCL 25 mg/day (PO)
and a short course of methtylprednisolon 32
mg/day (PO) were ordered to prevent the
frequency of relapses in patients. A discharge plan
was provided for patient that reduce the chance
of recurrence and reduce the frequency and
severity of future episodes and how to avoid
future exposure to the causative agent, if
possible. The patient was evaluated ten days after
the episode again, no any signs of allergic
reactions were found.
DISCUSSION
Anaphylaxis is the most severe life-threatening
form of a systemic allergic reaction10,11. The basic
mechanism underlying allergic reactions is mast
cell and basophil degranulation and mediator
release. The causes of cell degranulation include
IgE
cross-linking,
complement
activation,
nonimmunologic or direct activation, modulation
of arachidonic acid metabolism, exercise or
temperature-dependent effects, and idiopathic
causes2. Although anaphylactic reactions are
extremely rare cases have been reported in
individuals immunized with toxoids12. Most of
these cases provide just a clinical description and
in only a few was the presence of IgE antibodies
studied3.4.7.12.
The prevalence of anaphylaxis ranges from as
high as 5 per 1000 to as low as 2 per 10,000 ED
visits13,14. The prevalence of less-severe allergic
reactions in the emergency department is much
higher, but data are infrequently reported. In the
vast majority of patients, signs and symptoms
begin within 60 min of exposure. In general, the
faster the onset of symptoms, the more severe
the reaction, as evidenced by the fact that onehalf of anaphylactic fatalities occur within the first
hour.
Currently, the most common causes of serious
anaphylaxis are drugs (Beta-Lactam antibiotics,
Acetylsalicylic
acid,
Trimethoprim-sulfamethoxazole, Vancomycin, Nonsteroidal anti-inflammatory
drugs, virtually any drug antibiotics), foods and
addıtıves (Shellfish, Soybeans, Nuts, Wheat, Milk,
Eggs, Salicylates, Seeds, Sulfites), and others
(Hymenoptera stings insect, parts and molds,
radiographic contrast, material Latex)10,15.
The clinical signs of systemic allergic reactions
include diffuse urticaria and angioedema. As we
found in our case; at times these major symptoms
are accompanied by any of the following: colic
pain in abdomen, nausea, vomiting, diarrhea,
bronchospasm, rhinorrhea, conjunctivitis, dysrhythmias, and/or hypotension. The diagnosis of
anaphylaxis is made by history and physical
examination.
The
differential
diagnosis
of
anaphylactic reactions is extensive including
vasovagal reactions, myocardial ischemia, arrhythmias, status asthmaticus, seizure, epiglottitis,
hereditary
angioedema,
foreignbody
airway
obstruction, mastocytosis, vocal cord dysfunction,
and non-IgE-mediated drug reactions10.
It is designated in reports that epinephrine is the
cornerstone
of
treatment
for
anaphylactic
reactions; however, research suggests that
epinephrine in anaphylaxis is underused10,14,16.
The present report describes the occurrence of an
anaphylaxis in a twenty-four year-old woman after
the simultaneous administration of the second
booster dose of dT vaccine. The symptoms
developed within 10 minutes after administration
and deteriorated rapidly.
As it is designated in Kemp et al. study10, the
second-line anaphylaxis treatments are corticosteroids and antihistamines. In our study we began
with corticosteroid and antihistamine-2 blocker
directly. We were hesitant to give intravenous
epinephrine because of the patient’s tachycardia
(124/min) and tremor. The shock was not
refractory to this treatment, and the systemic
reaction improved within 30 min after the
treatment applied. Our patient needed only a
single dose of corticosteroid and antihistamine for
treatment.
Treatment in the outpatient setting should include
antihistamines and a short course of corticosteroids, although the evidence for this is weak17.
Our
study
demonstrates
that,
although
epinephrine is the first drug for treatment of
anaphylaxis, corticosteroids can be useful and can
treat anaphylaxis with antihistamines. The
treatment of an anaphylaxis may not finish at ED;
emergency physicians should provide discharge
plans for patients that reduce the chance of
recurrence and reduce the frequency and severity
of future episodes.
A brief limitations section: It was not possible
to do a detailed study to establish the causal
agent or agents in our hospital. (I saw this case in
Batman State Hospital seven months ago. At that
time I worked there). Although, we treated our
187
B. Al and C. Yıldırım
case with corticosteroid and antihistamine; we
don’t propose this treatment for anaphylaxis at
first. Epinephrine is the first preference;
corticosteroid and antihistamine are alternative
treatment.
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Correspondence:
Behçet AL, M.D.
Gaziantep University Faculty of Medicine Gaziantep
e-mail:[email protected]
Received
: 30.06.2008
Acceptance date : 29.07.2008