CASE REPORT

Electroconvulsive Therapy in a Patient With a
Recent Subarachnoid Hemorrhage
Seshagiri Rao Doddi, MBBS, Matthew Lotz, BS, William T. Regenold, MDCM, and Lawrence Adler, MD

Abstract: The safety of electroconvulsive therapy (ECT) is improving
with advances in anesthesia and ECT technique. There are published case
reports of successful treatment of depression in patients who were once
considered at high medical risk. Recent cerebral hemorrhage is one of
the conditions considered to significantly increase the risk of ECT treatment. Literature search did not indicate any case reports of ECT treatment
in patients with recent subarachnoid hemorrhage. We report the successful
ECT treatment of depression in an older man who had developed a subarachnoid hemorrhage after a suicide attempt by ingestion of antifreeze.
Key Words: electroconvulsive therapy, ECT, subarachnoid hemorrhage,
depression, older adult, ethylene glycol, suicide
(J ECT 2017;00: 00–00)

E

lectroconvulsive therapy (ECT) is a safe and effective treatment for patients experiencing a major depressive episode.1–4
Recent review articles suggest that the safety of ECT has been
enhanced over decades because of improvements in anesthesia
and ECT techniques with decreasing rates of medical morbidity
and mortality due to ECT treatments.4–6 These improved outcomes apply even to patients who were once considered high
risk for ECT. For example, case reports show that ECT can be
safely used to treat depression in patients with recent myocardial
infarction,7 severe thrombocytopenia,8 severe hemophilia,9 brain
aneurysms,10–13 repaired arteriovenous malformations,14 intracranial tumors,15 intracranial arachnoid cysts,16 and subdural
hemorrhage.17 On the other hand, there are also case reports of
intracerebral hemorrhage and subdural hematoma after ECT that
suggest that individuals with recent intracerebral bleeds are at
risk for further bleeding.17–20 A literature search using Medline,
PubMed, and PsycINFO did not reveal any reports of ECT treatment in patients with a recent subarachnoid hemorrhage. Here,
we report a case of an older adult with major depression who
sustained a subarachnoid hemorrhage and was successfully treated
with ECT.

CASE REPORT
Mr Z, a 72-year-old married white man, presented with a
6-month history of major depression. His depressive symptoms
included persistent and pervasive depressed mood, anhedonia,
loss of appetite, decreased energy, inappropriate guilt, feelings
of hopelessness and helplessness, and preoccupation with death
and suicidal ideas. His depression occurred in the context of multiple stressors including chronic pain, physical disability, and
financial concerns.
From the Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD.
Received for publication June 13, 2017; accepted July 21, 2017.
Reprints: Seshagiri Rao Doddi, MBBS, Department of Psychiatry, University of
Maryland Medical Center, Room No. S12 A05, 22 South Greene St,
Baltimore, MD 21201 (e‐mail: sdoddi@som.umaryland.edu).
The authors have no conflicts of interest or financial disclosures to report.
Copyright © 2017 Wolters Kluwer Health, Inc. All rights reserved.
DOI: 10.1097/YCT.0000000000000453

Journal of ECT • Volume 00, Number 00, Month 2017

Mr Z had no previous psychiatric history and no history of
alcohol or substance use. His past medical history was notable
for prostate cancer treated 16 years ago by prostatectomy with
resulting incontinence and erectile dysfunction; a lumbar back injury from a fall resulting in chronic pain, numbness, and weakness
in his legs with impaired gait requiring a walker, unrelieved by a
L4 to L5 fusion surgery several months before admission; mild
hypertension treated with amlodipine 2.5 mg daily, and gastroesophageal reflux disease treated with pantoprazole 20 mg daily.
During the second month of his depressive episode, Mr Z
made his first suicide attempt by ingesting antifreeze and making
multiple deep cuts on several parts of his body. A computerized
tomography (CT) scan of his head after this first suicide attempt
was read as normal with no evidence for an acute intracranial
bleed, acute ischemia, or mass effect. He was treated as an inpatient for 15 days at the Shock Trauma Center (STC) of the University of Maryland Medical Center. After he was extubated, he was
seen by psychiatric consultants who did not start any psychiatric
medications at that time because of resolving delirium. After medical management and surgical repair of muscles and tendons, he
was transferred to an acute rehabilitation facility. He was closely
followed by psychiatric consultants who started escitalopram
10 mg daily, which was titrated to 20 mg per day. He also received
individual therapy and showed significant improvement in his depressive symptoms. He was discharged home 2 months after his
initial suicide attempt and was referred for outpatient psychiatric
treatment. He saw a psychiatrist and a psychotherapist as an outpatient but did not fully comply with escitalopram therapy. He relapsed and made a second suicide attempt 4 months after his
discharge from the rehabilitation facility.
Mr Z was found by neighbors in his backyard lying unresponsive with an empty antifreeze container next to him. He was
taken to a local hospital emergency room by ambulance where
he was intubated. Physical examination did not show any bruises,
bumps, or external evidence of trauma to his head. A CT scan of
the head showed subarachnoid hemorrhage over the left parietal
and temporal lobes with no mass effect. The same day, he was
transferred to the STC of the University of Maryland Medical
Center from the local hospital for further medical management.
A repeat head CT scan on the day after admission to the STC
showed unchanged volume and distribution of subarachnoid blood
over the left parietal and temporal lobes without evidence of interval recurrent intracranial hemorrhage (Fig. 1). He also experienced
multiple metabolic and toxic effects due to the ethylene glycol
contained in antifreeze, including hypernatremia, hyperkalemia,
hyperlactemia, hyperosmolarity, and severe metabolic acidosis.
In the STC, he remained intubated with mechanical ventilation.
As per advise of poison control, he was treated for 48 hours with
fomepizole (4-methylpyrazole), which blocks the breakdown of
ethylene glycol into its toxic metabolites. He received multiple
rounds of hemodialysis for treatment of metabolic acidosis and
acute renal failure. After medical stabilization and extubation,
he was evaluated by the psychiatry consult service. One week
after his initial admission, he was transferred to the Older Adult
Psychiatric Inpatient Unit.
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Journal of ECT • Volume 00, Number 00, Month 2017

Doddi et al

FIGURE 1. Noncontrast CT scan of the patient’s head. A, The day
of suicide attempt. Hyperintensities in left temporoparietal region
indicate subarachnoid hemorrhage. B, Three days before first ECT.
No evidence of subarachnoid hemorrhage.

other acute intracranial process. Neurological assessments were
performed every 15 minutes up to 2 hours after each ECT treatment. The patient tolerated the ECT treatments without complications. Montgomery-Asberg Depression Rating Scale (MADRS)
and Mini-Mental Status Examination (MMSE) were administered
once before ECT treatment, on a weekly basis during ECT treatments, and after the ECT treatment to monitor for changes in severity of depression and cognition, respectively. The patient
showed dramatic improvement over the course of ECT treatment,
which was reflected in a decrease of MADRS score from 34 pretreatment to 5 posttreatment, indicating remission of his depression (Table 1). There were no significant changes noted in the
MMSE, which ranged from 28 to 30 (Table 1). The patient was
discharged home in stable condition with outpatient psychiatric
and medical follow-up. Mr Z was contacted by phone 5 months
after his discharge from the psychiatry unit. He reported continuing escitalopram 20 mg daily, seeing a psychiatrist regularly, and
maintaining sustained remission of his depression.

DISCUSSION
Upon admission to the psychiatric unit, he remained severely
depressed with all symptoms of depression noted earlier as well as
psychomotor retardation, a nihilistic delusion that he was hopelessly impoverished, and regret over not succeeding in his suicide
attempts. Electroconvulsive therapy was considered, but because
of his recent subarachnoid hemorrhage, he was deemed too high
risk for ECT, because an extension of his bleed could result in a
mass effect and possibly a catastrophic increase in intracranial
pressure. He was restarted on escitalopram, and the dose was
quickly increased to 20 mg per day. He received individual,
group, and milieu therapies. Over 4 weeks on the inpatient unit,
he showed minimal improvement. Despite frequent reviews by
his managed care company encouraging discharge to outpatient
treatment, he was considered to be at too high risk for suicide because of his recent attempts and multiple suicide risk factors
including advanced age, male sex, social isolation, psychosis,
strong family history of depression and suicide, chronic medical
illness and pain, and financial stressors. Electroconvulsive therapy
was therefore reconsidered.
To fully assess the current risks of ECT, a repeat head CT and
a neurosurgery consult were obtained. The head CT 30 days after
his initial CT showed interval resolution of the subarachnoid hemorrhage over the left parietal and temporal lobes with no evidence
of new hemorrhage (Fig. 1). The neurosurgery team agreed with
our assessment that the possible benefit of ECT for this patient
at high risk for suicide now outweighed the risk of a possible
new hemorrhage with ECT. The patient and family were informed
of the increased risk for adverse events with ECT treatment because of the recent subarachnoid hemorrhage. The patient provided written informed consent, and the family gave verbal
assent for ECT. His first treatment occurred 33 days after his
subarachnoid hemorrhage was seen on CT scan. Over the next
3 weeks, the patient was continued on escitalopram 20 mg per
day and was treated with a total of 9 bifrontal ECT treatments
using a Thymatron System IV device (Somatics, LLC, Lake
Bluff, Ill). Device settings were as follows: pulse width = 0.5 ms;
frequency = 30 Hz; stimulus duration, 5.6 to 6.5 seconds; total energy = 35 to 40 J; and charge = 150.6 to 178.5 mC. Methohexital
70 mg and succinylcholine 60 mg were administered intravenously for anesthesia and neuromuscular blockade, respectively,
before stimulation. Labetolol 15 to 20 mg intravenously was given
before stimulation to prevent a large increase in blood pressure. A
CT scan of the head was repeated after the first procedure to assess
for bleeding, which showed no intracranial hemorrhage or any

2

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To our knowledge, this is the first report of ECT performed
on a patient with a recent subarachnoid hemorrhage. With regard
to the cause of this patient's subarachnoid hemorrhage, it is noteworthy that this patient attempted suicide by ingestion of antifreeze. Ethylene glycol is one of the ingredients of antifreeze,
and its metabolites cause metabolic acidosis and result in formation of calcium oxalate crystals. The metabolites and calcium
oxalate crystals cause toxicity resulting in acute renal failure,
metabolic acidosis, and central nervous system toxicity.21–24 Intracerebral bipallidal hemorrhage has been reported with ethylene glycol ingestion and is hypothesized to be related to the
deposition of oxalate crystals.21 We verified that the antifreeze
used in the suicide attempt contained ethylene glycol and not
methanol, which is another possible ingredient of antifreeze that
has been associated with subarachnoid hemorrhage.25,26 Trauma
was considered an unlikely cause of the hemorrhage because examination revealed no evidence of head trauma. Rupture of a
blood vessel, such as an arteriovenous malformation or cerebral
aneurysm, was also deemed unlikely because of the small size
and lack of progression of the hemorrhage, although it could
not be definitively excluded because the patient did not have a
cerebral angiogram.
Active cerebral hemorrhage and recent cerebrovascular accident are considered relative contraindications to ECT.27,28 During
ECT treatment, there is an initial brief parasympathetic response
after electrical stimulation. This is followed by a sympathetic response associated with a hyperdynamic state that is characterized
by arterial hypertension, tachycardia, and considerably increased
cerebral blood flow rate and velocity.29,30 These responses lead
to a concern for increased risk of intracranial hemorrhage in
TABLE 1. MADRS and MMSE Scores Before, During, and
After ECT
MADRS and MMSE Scores Over ECT Course
Time
Pre-ECT
Week 1
Week 2
Week 3
Week 4 (post-ECT)

MADRS

MMSE

34
30
20
7
5

29
29
30
28
29

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Journal of ECT • Volume 00, Number 00, Month 2017

vulnerable patient populations. Administering ECT treatment after recent cerebrovascular hemorrhage increases the risk for new
hemorrhage and therefore requires careful assessment of risks
and benefits. In the case of this patient, the likely benefit of relieving his depression and the extremely high risk of suicide without
depression relief outweighed the risk of morbidity and mortality
associated with renewed subarachnoid hemorrhage in light of
hemorrhage resolution and advice from the neurosurgery team.
In sum, this case illustrates that ECT can be administered safely
to a patient 33 days post–subarachnoid hemorrhage without mass
effect by taking essential precautions including follow-up brain imaging, neurosurgical consultation, and the use of β-blocker medication (eg, labetolol) to minimize the risk of intracranial hemorrhage
associated with hemodynamic changes accompanying ECT.
REFERENCES

ECT in Patient With Recent Subarachnoid Hemorrhage

14. Marks JA, Bryson EO, Adams DA, et al. The safe use of electroconvulsive
therapy in a patient with a repaired arteriovenous malformation: images
showing surgical clips. J ECT. 2016;32:3–4.
15. Geduldig ET, Kellner CH. Electroconvulsive therapy in the elderly: new
findings in geriatric depression. Curr Psychiatry Rep. 2016;18:40.
16. Desseilles M, Thiry J, Monville J, et al. Electroconvulsive therapy for
depression in a patient with an intracranial arachnoid cyst. J ECT. 2009;25:
64–66.
17. Wijeratne C, Shome S. Electroconvulsive therapy and subdural
hemorrhage. J ECT. 1999;15:275–279.
18. Weisberg LA, Elliott D, Mielke D. Intracerebral hemorrhage following
electroconvulsive therapy. Neurology. 1991;41:1849.
19. Kulkarni RR, Melkundi S. Subdural hematoma: an adverse event of
electroconvulsive therapy-case report and literature review. Case Rep
Psychiatry. 2012;2012:585303.

1. Fink M. Convulsive therapy: a review of the first 55 years. J Affect Disord.
2001;63:1–15.

20. Saha D, Bisui B, Thakurta RG, et al. Chronic subdural hematoma following
electro convulsive therapy. Indian J Psychol Med. 2012;34:181–183.

2. van der Wurff FB, Stek ML, Hoogendijk WJ, et al. The efficacy and safety
of ECT in depressed older adults: a literature review. Int J Geriatr
Psychiatry. 2003;18:894–904.

21. Caparros-Lefebvre D, Policard J, Sengler C, et al. Bipallidal haemorrhage
after ethylene glycol intoxication. Neuroradiology. 2005;47:105–107.

3. Abrams R. The mortality rate with ECT. Convuls Ther. 1997;13:125–127.
4. Watts BV, Groft A, Bagian JP, et al. An examination of mortality and other
adverse events related to electroconvulsive therapy using a national adverse
event report system. J ECT. 2011;27:105–108.
5. Rice EH, Sombrotto LB, Markowitz JC, et al. Cardiovascular morbidity in
high-risk patients during ECT. Am J Psychiatry. 1994;151:1637–1641.
6. Nuttall GA, Bowersox MR, Douglass SB, et al. Morbidity and mortality in
the use of electroconvulsive therapy. J ECT. 2004;20:237–241.
7. Magid M, Lapid MI, Sampson SM, et al. Use of electroconvulsive therapy
in a patient 10 days after myocardial infarction. J ECT. 2005;21:182–185.
8. Gonzalez-Arriaza HL, Mueller PS, Rummans TA. Successful
electroconvulsive therapy in an elderly man with severe thrombocytopenia:
case report and literature review. J ECT. 2001;17:198–200.

22. Barceloux DG, Krenzelok EP, Olson K, et al. American Academy of
Clinical Toxicology Practice Guidelines on the treatment of ethylene
glycol poisoning. Ad Hoc Committee. J Toxicol Clin Toxicol. 1999;37:
537–560.
23. Battistella M. Fomepizole as an antidote for ethylene glycol poisoning.
Ann Pharmacother. 2002;36:1085–1089.
24. Baud FJ, Galliot M, Astier A, et al. Treatment of ethylene glycol poisoning
with intravenous 4-methylpyrazole. N Engl J Med. 1988;319:97–100.
25. Askar A, Al-Suwaida A. Methanol intoxication with brain hemorrhage:
catastrophic outcome of late presentation. Saudi J Kidney Dis Transpl.
2007;18:117–122.
26. Aisa TM, Ballut OM. Methanol intoxication with cerebral hemorrhage.
Neurosciences (Riyadh). 2016;21:275–277.

9. Saito N, Shioda K, Nisijima K, et al. Second case report of successful
electroconvulsive therapy for a patient with schizophrenia and severe
hemophilia A. Neuropsychiatr Dis Treat. 2014;10:865–867.

27. American Psychiatric Committee on Electroconvulsive Therapy.
The Practice of Electroconvulsive Therapy: Recommendations for
Treatment, Training and Privileging. 2nd ed. Washington, DC: American
Psychiatric Association Publishing; 2001.

10. Leonard SD. Electroconvulsive therapy and intracranial aneurysms.
Proceedings of UCLA Healthcare. 2016;20.

28. Waite J, Easton A. The ECT Handbook. 3rd ed. London, UK: Royal
College of Psychiatrists Publications; 2013.

11. Bader GM, Silk KR, Dequardo JR, et al. Electroconvulsive therapy and
intracranial aneurysm. Convuls Ther. 1995;11:139–143.
12. Drop LJ, Viguera A, Welch CA. ECT in patients with intracranial
aneurysm. J ECT. 2000;16:71–72.

29. Viguera A, Rordorf G, Schouten R, et al. Intracranial haemodynamics
during attenuated responses to electroconvulsive therapy in the presence
of an intracerebral aneurysm. J Neurol Neurosurg Psychiatry. 1998;64:
802–805.

13. van Herck E, Sienaert P, Hagon A. Electroconvulsive therapy for patients
with intracranial aneurysms: a case study and literature review. Tijdschr
Psychiatr. 2009;51:43–51.

30. Viguera A, Welch C, Bigatello L, et al. Hemodynamic responses to
electroconvulsive therapy in a hypertensive patient with end-stage
pulmonary fibrosis. Anesth Analg. 1998;87:737–741.

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