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General Hospital Psychiatry 34 (2012) 703.e9 – 703.e11

Case Report

Acute neurogenic pulmonary edema following electroconvulsive therapy:

a case report
Tohru Takahashi, M.D., Ph.D. a,⁎, Kuni Kinoshita, M.D. a , Tomonori Fuke, M.D. a ,
Kazuhisa Urushihata, M.D. b , Tomoyuki Kawamata, M.D., Ph.D. c , Shin Yanagisawa, M.D. d ,
Tomoki Kaneko, M.D. d , Shinsuke Washizuka, M.D., Ph.D. a ,
Tokiji Hanihara, M.D., Ph.D. e , Naoji Amano, M.D., Ph.D. a
a
Department of Psychiatry, Shinshu University School of Medicine, Nagano, Japan
b
First Department of Internal Medicine, Shinshu University School of Medicine, Nagano, Japan
c
Department of Anesthesiology and Resuscitology, Shinshu University School of Medicine, Nagano, Japan
d
Department of Radiology, Shinshu University School of Medicine, Nagano, Japan
e
School of Health Sciences, Shinshu University, Nagano, Japan
Received 28 October 2011; revised 7 March 2012; accepted 7 March 2012

Abstract

Objective: We report the case of a 47-year-old man with depression who developed acute dyspnea, hypoxemia, and mild hemoptysis after
electroconvulsive therapy (ECT).
Method: Intravenous carbazochrome sodium sulfate hydrate as a hemostatic drug (100 mg/day) was prescribed for 2 days. On the day of
ECT, oxygen inhalation (4 L/min) was continued, and SpO2 was maintained at 94–96%.
Results: Chest radiography showed improvement in alveolar infiltration. Chest CT 6 days after ECT also confirmed the disappearance of
ground glass opacities in the lung fields.
Conclusion(s): NPE is lifethreatening and should be recognized as an uncommon adverse event associated with ECT.
© 2012 Elsevier Inc. All rights reserved.

Keywords: Neurogenic pulmonary edema; Electroconvulsive therapy; Side effect; Epileptic seizure

1. Introduction the case of a patient with depression who developed acute

Neurogenic pulmonary edema (NPE) is a life threatening
complication that can follow severe central nervous system
injury. NPE typically develops rapidly following the injury
and is characterized by an increase in pulmonary interstitial
and alveolar congestion. The exact pathophysiological
mechanism(s) leading to NPE remain unclear [1–3]. Both
the release of vasoactive substances and rapid and transient
sympathetic discharge are thought to be involved [2,3]. The
primary precipitants of NPE are subarachnoid hemorrhage,
severe traumatic head injury, or, occasionally, epilepsy
[1–5]. Few reports of NPE related to electroconvulsive
therapy (ECT) have been reported thus far [6–8]. We report
⁎ Corresponding author. Tel.: +81 263 37 2638; fax: +81 263 36 1772.
E-mail address: takatoh@shinshu-u.ac.jp (T. Takahashi).
0163-8343/$ – see front matter © 2012 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.genhosppsych.2012.03.004
dyspnea, hypoxemia, and mild hemoptysis after ECT.
1.1. Case report
A 47-year-old man was admitted for recurrent depression.
At the age of 43, he experienced his first episode of
depression. At age 45, he was admitted due to recurrence and
underwent ECT 4 times. At that time, ECT was performed
using propofol as a venous anesthesia, suxamethonium as a
muscle relaxant, and a pulse wave ECT device at a maximum
output of 35%. No complications were noted. Two years
later, he developed a depressive mood and suicidal ideation
again. He requested ECT and was admitted.
On admission, chest radiography and electrocardiography
were unremarkable. Blood analysis revealed elevated liver
enzymes and hyperlipidemia. Abdominal computed tomog-
raphy (CT) revealed a fatty liver.
703.e10 T. Takahashi et al. / General Hospital Psychiatry 34 (2012) 703.e9–703.e11
The first ECT was performed 6 days after admission.
Venous anesthesia (thiopental) and a muscle relaxant
(suxamethonium) were administered by an anesthesiolo-
gist. Using the titration method, bilateral stimulation was
performed using a pulse wave ECT device (Thymatron
System IV) at a starting stimulus dose of 20%, followed
by 10% increments. Stimulation at 20% and 30% did not
induce convulsion. The third electric stimulation at a dose
of 40% induced a convulsion that lasted 33 s. During ECT,
the systolic blood pressure was 140 mm Hg, and the
maximum cardiac rate was 130 beats/min. Percutaneous
oxygen saturation (SpO2) was maintained at 100%.
After ECT, oxygen inhalation (5 L/min) was continued.
About 30 min after ECT, SpO2 decreased to 77%, and
oxygen was increased to 7 L/min. About 3 h after ECT,
dyspnea and a small amount of hemoptysis were observed.
The SpO2 level decreased to 89%. Coarse crackles were
diffusely audible in both the lungs. Blood gas analysis under
oxygen inhalation (2 L/min) showed an arterial partial
pressure of oxygen (PO2) of 68.5 mm Hg, arterial partial
pressure of carbon dioxide (PCO2) of 35.6 mm Hg, and pH
of 7.38. The white blood cell count was 12,450 cells/μL and
the C-reactive protein (CRP) level was 0.30 mg/dL. Chest
radiography revealed alveolar infiltration predominantly on
the central side in both the lungs and a normal-sized heart.
Chest CT performed on the same day showed multiple
nodules with ground glass opacity in both the lungs,
suggesting alveolar bleeding (Fig. 1A). A diagnosis of
NPE was made. Intravenous carbazochrome sodium sulfate
hydrate as a hemostatic drug (100 mg/day) was prescribed
for 2 days. On the day of ECT, oxygen inhalation (4 L/min)
was continued, and SpO2 was maintained at 94–96%, after
which dyspnea disappeared. The next day, under oxygen
inhalation (1 L/min), SpO2 was maintained at 97%. Blood
examination showed a white blood cell count of 6,630
cells/μL and a CRP level of 1.31 mg/dL. There was no
evidence of collagen vascular disease. Two days after ECT,
oxygen inhalation was discontinued, and SpO2 was main-
Fig. 1. Chest computed tomography (A) 6 hours after ECT and (B) 6 days after ECT.
tained at ≥96%. Chest radiography showed improvement in
alveolar infiltration. Chest CT 6 days after ECT also
confirmed the disappearance of ground glass opacities in
the lung fields (Fig. 1B).
2. Discussion
NPE is an acute pulmonary edema secondary to severe
central nervous system insult, characterized by marked
pulmonary vascular congestion with perivascular edema,
extravasation and intra-alveolar accumulation of protein-rich
fluid, and intra-alveolar hemorrhage [1,2]. The exact
pathophysiological mechanism underlying NPE is not fully
understood, although 2 separate mechanisms are suggested:
systematic and massive centrally mediated adrenergic
excitation-induced pulmonary vasoconstriction, and an
increase in both pulmonary hydrostatic pressure and the
permeability of pulmonary capillaries [1–3]. The perme-
ability defects are probably mediated by the adrenergic tone
or by the release of a second mediator (e.g., endorphins,
histamine, or bradykinin) [3]. An initial rapid increase in
hydrostatic pressure may cause pulmonary microvascular
injury resulting in a permeability defect that is aggravated by
additional inflammation [2,3,9]. In cases of epilepsy, NPE
generally occurs during the postictal period and may occur
repeatedly [2,4,10]. However, to the best of our knowledge,
there have been only 4 reported cases of NPE after ECT,
including ours. Buisseretwas the first to report the case of a
woman with depression who developed difficulty breathing 1
h after ECT and eventually died of cardiopulmonary arrest 16
h after ECT [6]. Tsutsumi et al.reported the case of a woman
with hypertension, in whom a second ECT session resulted in
NPE requiring mechanical ventilation for 4 days [7]. Price et
al.reported the case of a man with hypertension, in whom
unilateral ECT performed 6 times caused no problems, but
the first bilateral ECT resulted in NPE [8]. In our patient, pre-
existing respiratory-circulatory complications were unre-
markable and 4 ECT sessions at another hospital did not
 T. Takahashi et al. / General Hospital Psychiatry 34 (2012) 703.e9–703.e11 703.e11

induce NPE. In our department, NPE developed immediately
after 3 consecutive titrating electric stimulations. The severity
of NPE after ECT varies [6–8] and the prevalence of NPE
after ECT is not known [11]. The occurrence of NPE after
ECT is difficult to predict, since most patients do not develop
NPE after their first ECT experience. The clinical diagnosis
of NPE is made by the temporal relationship of the pulmonary
edema to the neurological insult and by the exclusion of other
causes of pulmonary edema. When respiratory symptoms
such as hypoxemia or hemoptysis develop after ECT, NPE
should be suspected, and chest radiography or chest CT is
crucial for diagnosis. To date, there are no interventions
known to be helpful in preventing the development of NPE.
NPE is treated in a supportive and conservative fashion, since
most cases resolve within several days [1–3].
[10] Darnell JC, Jay SJ. Recurrent postictal pulmonary edema: a case report
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