Reminder of important clinical lesson

Delayed diagnosis of a cerebrovascular accident associated
with anabolic steroid use
Isabelle Cooper, Nina Reeve, Warren Doherty
Department of Anaesthetics, Cheltenham General Hospital, Cheltenham, UK
Correspondence to Dr Isabelle Cooper, isabellecooper@doctors.org.uk

Summary
The authors report a case of atherosclerotic stroke in a 46-year-old recreational bodybuilder with a 20 year history of anabolic-adrenergic
steroid (AAS) abuse. Cerebrovascular accident (CVA) occurred during his third week of hospital admission for an acute abdomen and on day
8, postemergency laparotomy. CVA presented with collapse, generalised seizures, reduced Glasgow Coma Score and severe hypertension.
He was subsequently admitted to the intensive care unit (ICU), where initial investigations did not illustrate an underlying diagnosis. By
day 4 in ICU, there had been no significant clinical improvement and radiological investigations were repeated, identifying a left frontal lobe
infarct in the middle cerebral artery territory. The authors propose CVA was secondary to AAS. After a prolonged and complicated period of
rehabilitation, he has been discharged home; he requires carers due to dyspraxia and is mobilising independently.

BACKGROUND
Anabolic-adrenergic steroids (AAS) are commonly being
self-administered in supraphysiological doses by recreational bodybuilders to increase muscle mass, strength and
enhance athletic performance. There are numerous multiorgan side effects of AAS abuse (table 1), many of which
are dose-related and reversible upon drug cessation.1
The authors report a case of stroke in a recreational
bodybuilder with a history of nandrolone abuse and drug
related co-morbidities: obstructive sleep apnoea (OSA),
chronic renal failure, osteoarthritis and depression with 3
prior suicide attempts.
Cerebrovascular accidents (CVA) are a rare, but significant risk of AAS and few reported cases of ischaemic
stroke in AAS users exist.2–5 This case is the first, to our
knowledge of ischaemic stroke in a nandrolone user. It
highlights the importance of recognition of AAS abuse in
patients and knowledge of the consequences.

CASE PRESENTATION
The patient, a 46-year-old recreational bodybuilder, had a
20 year history of nandrolone abuse, alongside intermittent use of growth hormone and testosterone. He injected
Deca-Durabolin, a form of nandrolone and would administer this in increasing doses over a 2–3 month period and
follow this ‘buildup cycle’ with a drug-free period. This
patient’s average dose of nandrolone varied enormously,
while the cyclical administration pattern remained continuous. At hospital admission, he weighed 134 kilograms
and had a well defined muscular physique.
Our patient was admitted to hospital twice within a
week; the first admission was for intravenous antibiotic
treatment of a lower limb cellulitis. He was discharged
home after 5 days and was readmitted 1 day later with
abdominal pain and severe sepsis. CT abdomen showed
acute cholecystitis and blood cultures were positive for
Escherichia coli. On the surgical ward, pain and pyrexia
persisted despite treatment and he was re-imaged 11 days
BMJ Case Reports 2011; doi:10.1136/bcr.02.2011.3857

later, when a perforated sigmoid diverticulum was identified. He was subsequently admitted to the intensive care
unit (ICU) following an emergency laparotomy. Pain control issues continued postoperatively and high doses of
morphine through a patient controlled analgesia device
were required to keep him comfortable. Hypertension was
an intermittent problem and it was felt that addressing his
pain was the optimum way to control his blood pressure.
Otherwise, he continued to make a good recovery and was
discharged to the surgical ward.
Three days later, he was readmitted to ICU following a
collapse with witnessed generalised seizures, a Glasgow
Coma Score of 3/15, hypoxia, tachycardia, severe hypertension and temperature of 38°C. He required immediate
intubation and ventilation for oxygenation.
Significant findings of initial investigations showed a
respiratory acidosis on blood gas analysis, white blood cell
count 44.3, C reactive protein 146 and troponin-T 1.3 with
a normal ECG and 24 h tape. Radiological investigations
included a normal CT head scan, a CT abdomen showing changes consistent with recent surgery and a CT pulmonary angiogram that showed features in keeping with
acute respiratory distress syndrome. He was subsequently
ventilated using high frequency oscillation for 12 h and
required 2 days of inotrope support.
Intermittent right-sided seizures persisted for 2 days
despite phenytoin therapy and were attributed to sepsis
and hypoxia. Sedation was turned off on day 4 and a neurological examination showed him to have right-sided upper
limb weakness (Medical Research Council (MRC) scale 0/5),
Table 1 Side effects of AAS7
Acne vulgaris
Dyslipidaemia
Cholestatic jaundice
Oligo-azospermia
Musculoskeletal: tendon injuries

Psychiatric: depression, psychosis
Glucose intolerance
Hepatocellular carcinoma
Painful gynaecomastia
Renal carcinoma

1 of 4

Figure 1

CT head showing left middle cerebral artery infarct.

that was greater than his lower limb (MRC scale 4/5), with
hypertonia, an extensor plantar response and right-sided
neglect. There was no response to antibiotics and a repeat
CT head scan revealed an extensive left frontal lobe infarct
in the middle cerebral artery (MCA) territory (figure 1).

being managed with lifelong warfarin in view of his second
thromboembolic event and pancreatitis, which was managed conservatively. He has now been discharged home,
where he is independently mobilising, but has residual
right upper limb weakness. His main problem is dyspraxia
and he requires carers to assist with functional daily tasks.

INVESTIGATIONS
Further investigations shed no light on the cause of CVA
and included a carotid artery duplex scan, a transoesophageal echo with bubble study, auto-antibody, lupus and
vasculitis screen. However, a lipid profile revealed total
cholesterol of 3.4 mmol/l (normal value <5 mmol/l) and
a raised low-density lipoprotein (LDL) cholesterol of 2.7
mmol/l (normal value <2.0 mmol/l).

DIFFERENTIAL DIAGNOSIS
Prior to obtaining the repeat CT head scan, underlying differential diagnoses included meningitis, encephalitis, central line, chest or abdominal sepsis.

OUTCOME AND FOLLOW-UP
After a prolonged stay on the stroke unit with extensive
rehabilitation, our patient unfortunately encountered further complications suffering a pulmonary embolism that is
2 of 4

DISCUSSION
The link between stanozolol and CVA has been recognised,
but to date there have been no case reports of nandrolone
and CVA. Nandrolone is the most commonly used injectable steroid and is a 17-β-ester testosterone derivative,
while stanozolol is a 17-α-alkyl testosterone derivative
and can be administered orally or intramuscularly.6 Risk of
CVA is enhanced with concurrent use of other doping substances.7 There have been no documented cases of CVA
in AAS users that have been concurrently administering
growth hormone or testosterone. Our patient had not used
growth hormone or testosterone within the year prior to
his CVA.
On admission, medical history included OSA, chronic
renal failure, osteoarthritis and depression. While these
co-morbidities are significant, none are known to have
causal links with CVA in this patient’s age group. OSA,
BMJ Case Reports 2011; doi:10.1136/bcr.02.2011.3857

osteoarthritis and depression have been associated with
AAS and it is likely they are secondary to nandrolone use
in this patient.7
Proposed mechanisms of AAS induced CVA includes
atherosclerosis, hyperhomocysteinemia, vasospasm and
platelet aggregation; complex interactions exist between
these four mechanisms.
Atherosclerosis occurs secondary to decreased high-density lipoprotein and increased LDL cholesterol in the presence of normal total cholesterol and triglyceride levels.6
Dyslipidemia results in endothelial dysfunction, increased
risk of atheroma formation and subsequently increased
risk of CVA. Our patient’s lipid profile illustrates a pattern
consistent with AAS use.
Increased homocysteine levels also impair endothelial
function. AAS users have significantly elevated levels of
homocysteine,8 which rise most significantly during the
higher dose phase of the AAS cycle.6 Graham et al, 2006
proposes homocysteine induces endothelial dysfunction
by generation of reactive oxygen species and the use of
antioxidants by AAS users may be beneficial in modifying
these effects.
Arterial vasospasm occurs due to excess LDL cholesterol
oxidising at the endothelium and inhibiting endothelial
nitric oxide release. Decreased nitric oxide production
impairs smooth muscle relaxation and vasodilatation.2 This
is a similar pathophysiological mechanism to that seen in
cocaine and nitric oxide, which is known to induce coronary artery vasospasm. Cocaine also affects other parts of
the circulation as illustrated by ischaemic damage to the
nasal septum. As the endothelial effects of nitric oxide are
similar throughout the vascular tree, such as glyceryl trinitrate induced headache, it seems likely AAS may cause cerebral artery vasospasm.
Effects on the haemostatic system increase the risk of
thrombosis formation. Decreased nitric oxide increases
endothelial production of thromboxane A2 and decreases
production of prostacyclin. This causes enhanced platelet sensitivity and aggregation, despite a normal platelet
count,2 8 and therefore increased CVA risk.
On a more positive note, AAS and in particular nandrolone, may have some beneficial effects when administered in low doses under medical supervision in the
management of isolated postoperative muscle wasting and generalised muscle wasting after periods of
immobilisation.
Greater knowledge and appreciation of AAS would have
altered our patient’s management and may have even prevented the CVA from occurring. Firstly, exploration of his
drug history and links with his co-morbidities did not take
place until his initial admission to ICU. This should have

BMJ Case Reports 2011; doi:10.1136/bcr.02.2011.3857

been explored on admission to hospital and resulted in
increased recognition of the severity of the patient’s condition and prompted earlier investigation. Secondly, more
aggressive management of his hypertension should have
occurred throughout hospital admission. Thirdly, an electroencephalograph should have been performed following
his collapse, as this may have revealed an ischaemic focus
prior to any radiological changes. Finally, with the above
knowledge, CVA as the unifying diagnosis should have
been considered earlier as a cause of collapse and thrombolysis administered despite relative contraindications.
This case is the first to demonstrate a link between nandrolone and CVA and adds to the mounting evidence in
the literature that cerebrovascular side effects of AAS must
be recognised. We have proposed four mechanisms linking
AAS and cerebrovascular morbidity; however, the pathogenesis is multifactorial and there is significant overlap
between each mechanism. It is clear that further research
is required to clarify the thrombogenicity of AAS and to
generate direct evidence of the effects on humans.

Learning points
Have a high index of suspicion for AAS abuse and
obtain detailed drug histories in a general practice and
hospital setting.
▶ Be aware of and recognise the multiple co-morbidities
associated with AAS use.
▶ When AAS abuse is known, actively look for other
co-morbidities and try to identify and modify risks.
▶

Competing interests None.
Patient consent Obtained.

REFERENCES
1. Hartgens F, Kuipers H. Effects of androgenic-anabolic steroids in athletes.
Sports Med 2004;34:513–54.
2. Santamarina RD, Besocke AG, Romano LM, et al. Ischemic stroke related to
anabolic abuse. Clin Neuropharmacol 2008;31:80–5.
3. Frankle MA, Eichberg R, Zachariah SB. Anabolic androgenic steroids and a
stroke in an athlete: case report. Arch Phys Med Rehabil 1988;69:632–3.
4. Akhter J, Hyder S, Ahmed M. Cerebrovascular accident associated with
anabolic steroid use in a young man. Neurology 1994;44:2405–6.
5. Laroche GP. Steroid anabolic drugs and arterial complications in an athlete–a
case history. Angiology 1990;41:964–9.
6. Kam PC, Yarrow M. Anabolic steroid abuse: physiological and anaesthetic
considerations. Anaesthesia 2005;60:685–92.
7. Quaglio G, Fornasiero A, Mezzelani P, et al. Anabolic steroids: dependence
and complications of chronic use. Intern Emerg Med 2009;4:289–96.
8. Graham MR, Grace FM, Boobier W, et al. Homocysteine induced
cardiovascular events: a consequence of long term anabolic-androgenic
steroid (AAS) abuse. Br J Sports Med 2006;40:644–8.

3 of 4

This pdf has been created automatically from the final edited text and images.
Copyright 2011 BMJ Publishing Group. All rights reserved. For permission to reuse any of this content visit
http://group.bmj.com/group/rights-licensing/permissions.
BMJ Case Report Fellows may re-use this article for personal use and teaching without any further permission.
Please cite this article as follows (you will need to access the article online to obtain the date of publication).
Cooper I, Reeve N, Doherty W. Delayed diagnosis of a cerebrovascular accident associated with anabolic steroid use. BMJ Case Reports 2011;
10.1136/bcr.02.2011.3857, date of publication
Become a Fellow of BMJ Case Reports today and you can:
▶ Submit as many cases as you like
▶ Enjoy fast sympathetic peer review and rapid publication of accepted articles
▶ Access all the published articles
▶ Re-use any of the published material for personal use and teaching without further permission

For information on Institutional Fellowships contact consortiasales@bmjgroup.com
Visit casereports.bmj.com for more articles like this and to become a Fellow

4 of 4

BMJ Case Reports 2011; doi:10.1136/bcr.02.2011.3857