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Resuscitation (2006) xxx, xxx—xxx
CASE REPORT
Pulmonary hypertension and predominant
right heart failure in thyrotoxicosis夽
Yael Paran a, Adi Nimrod b, Yelena Goldin a, Dan Justo a,∗
a
Department of Internal Medicine D,
Tel-Aviv Sourasky Medical Center, Weizman 6 Street, Tel Aviv 64239, Israel
b Department of General Intensive Care, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel
Received 8 April 2005 ; received in revised form 20 August 2005; accepted 2 September 2005
KEYWORDS
Resuscitation;
Pulmonary
hypertension;
Heart failure;
Amiodarone
Summary In this report we discuss a patient with predominant right heart failure and pulmonary hypertension, caused by thyrotoxicosis due to Graves disease,
which deteriorated to asystole, due to amiodarone administration for rapid atrial
fibrillation.
© 2005 Elsevier Ireland Ltd. All rights reserved.
Introduction
Pulmonary hypertension is not a recognized complication of thyrotoxicosis,1 although there are
few reports describing this phenomenon. In most
of these reports, the course of events was not
life threatening following adequate treatment for
thyrotoxicosis.2—9
Amiodarone is used to reduce ventricular
rate response in rapid paroxysmal atrial fibrillation (RPAF).10 Amiodarone may also induce
thyrotoxicosis,11 which might trigger or worsen
RPAF.10 Thus, many physicians advise against giving
amiodarone for RPAF in urgent situations without
first excluding thyrotoxicosis, because other agents
are available to treat RPAF.12
夽 A Spanish translated version of the summary of this article appears as Appendix in the online version at 10.1016/j.
resuscitation.2005.09.002.
∗ Corresponding author. Tel.: +972 97408575;
fax: +972 97408575.
E-mail address: [email protected] (D. Justo).
Pulmonary hypertension secondary to thyrotoxicosis, which deteriorated to heart failure and asystole after amiodarone administration has not been
reported so far. We wish to raise the level of awareness of the possibility of pulmonary hypertension
in thyrotoxicosis and the dangers of amiodarone
administration for RPAF without first excluding thyrotoxicosis.
Case report
A 38-year-old unconscious Philippine female was
admitted to the emergency room with hypoglycaemia (30 mg/dL). Consciousness returned
following intravenous glucose administration. The
ECG showed rapid atrial fibrillation and she was
treated with an intravenous bolus of amiodarone
by the paramedics. Her medical history revealed
a thyroidectomy a few years earlier for an unclear
indication. She did not return for further follow-up
although she had palpitations, probably due to
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a lack of medical insurance, being an illegal
employee in Israel. Physical examination revealed
dyspnoea, diaphoresis, jaundice, high fever, distended jugular veins, hepatomegaly, ascites, ankle
oedema and diffuse bilateral rales on auscultation
of the chest. A chest roentgenogram showed
prominent vascular marking. Laboratory tests
yielded leukocytosis with neutrophilia, mildly
elevated cellular liver enzymes, mild unconjugated
bilirubinaemia, and a prolonged prothrombin time
and partial prothrombin time. The patient was
given oxygen through a facial mask, intravenous
furosemide for pulmonary congestion and intravenous ceftriaxone as an empirical treatment for
aspiration pneumonia.
An hour later, the patient deteriorated to asystole requiring prolonged cardiopulmonary resuscitation before a return of spontaneous circulation.
Further laboratory tests yielded an undetectable
(<0.01 mU/L) serum level of thyroid-stimulating
hormone (TSH), free thyroxin (FT4) serum level of
10.9 ng/dL (normal, 0.7—1.8 ng/dL) and a total triiodothyronine (TT3) serum level of 638 ng/dL (normal, 80—200 ng/dL). Anti-thyroid peroxidase antibodies were positive at 803.0 U/mL. The diagnosis
of thyrotoxicosis (Grave’s disease) was established
and the patient was started on propranolol, propylthiouracil and dexamethasone.
Two hours later, the patient underwent a
transthoracic echocardiogram which revealed a
dilated right ventricle, general reduced right ventricle systolic function, severe elevated systolic
pulmonary artery pressure of 70 mmHg and moderate tricuspid valve regurgitation. The left ventricle was normal sized with an ejection fraction of
55% (Figure 1). A ventilation—perfusion pulmonary
Figure 1 A transthoracic echocardiogram revealing a
dilated right ventricle and tricuspid valve regurgitation
consistent with high systolic pulmonary artery pressure.
Y. Paran et al.
scan demonstrated a low probability for pulmonary
embolism.
During the following days the patient’s clinical
condition improved gradually and she was extubated. Two weeks later, a second transthoracic
echocardiogram was performed revealing a normal
sized right ventricle with normal systolic function,
mild elevated systolic pulmonary artery pressure
of 48 mmHg and mild tricuspid valve regurgitation.
Finally, the patient was discharged and visited our
outpatient clinic several weeks later with no signs
or symptoms of heart failure and in good clinical
condition. TSH, FT4 and TT3 serum levels were also
within the normal laboratory range.
Discussion
Pulmonary hypertension is defined as a mean pulmonary artery pressure higher than 25 mmHg at
rest.1 There are few reports on pulmonary hypertension secondary to thyrotoxicosis2—9 ; excess thyroid hormone might cause pulmonary hypertension
by increasing the cardiac output and by constricting
the pulmonary artery.13 In most of these reports,
thyrotoxicosis is due to Grave’s disease 2—9 ; thyroid auto-antibodies secreted in Grave’s disease
might injure the pulmonary endothelium, further
contributing to pulmonary hypertension.9 Nevertheless, pulmonary hypertension is not recognized
as a complication of thyrotoxicosis,1 probably due
to the favourable outcome described in previous
reports.2—9 We wish to raise the level of suspicious
for pulmonary hypertension secondary to thyrotoxicosis, in light of our experience.
Amiodarone is a class III anti-arrhythmic agent
which prolongs AV nodal conduction and is used to
lower ventricular rate response in RPAF.10 Amiodarone, which has a high iodine content, might
induce thyrotoxicosis by loading iodine on the
thyroid gland and by inducing a thyroiditis-like
condition,11 and in turn, may trigger or worse
RPAF.10 This is of significance, since 6.2% of the
patients who present to an emergency department
with RPAF also have thyrotoxicosis.14 Amiodarone
is generally considered to be contraindicated in
patients with RPAF secondary to thyrotoxicosis and
there are strong opinions against empirical administration of amiodarone for RPAF without first excluding thyrotoxicosis.12 We join these calls and ask for
more careful use of amiodarone.
This presentation of thyrotoxicosis was mainly
due to an untreated Grave’s disease and associated with the administration of amiodarone. The
consequences of health neglect due to lack of med-
Pulmonary hypertension and predominant right heart failure in thyrotoxicosis
ical insurance are frequently seen in the emergency
departments. There is a large population of foreign
employees in Israel, particularly in Tel-Aviv, most
of whom are hiding from the emigration authorities
and do not have medical insurance. These circumstances are also prevalent in other cities in developed countries. Unfortunately, only severe distress
brings these poor people to seek medical treatment.
Conclusions
Pulmonary hypertension and heart failure in a
patient with neglected Grave’s disease deteriorating to cardiopulmonary collapse, associated with
the administration of amiodarone, have not been
reported yet. We wish to raise the level of awareness of this complication in patients with pulmonary
hypertension and thyrotoxicosis and the danger of
amiodarone administration without first excluding
thyrotoxicosis.
Conflict of interest statement
None.
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