We present a case of extreme bradycardia in an 18-year-old man, accompanied by bilateral pleural effusions, pericardial effusion, endocrine dysregulation and Horner’s syndrome. Despite extensive investigations as an inpatient and multidisciplinary input, it was not until subsequent assessment by an endocrine team that it was revealed that his presentation was attributable to an eating disorder. Following dietary advice, easing of extreme exercise and continued support, the patient improved in all parameters including body mass index and he remains well. This case demonstrates the importance of a thorough personal history incorporating all aspects of social and dietary history.
- cardiovascular medicine
- nutrition and metabolism
- eating disorders
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Many cases of eating disorder are undetected, particularly if they present to a specialty unfamiliar with them. Eating disorders have profound effects on the cardiovascular system and carry a significant risk through arrhythmia, bradycardia, hypotension and heart failure, so prompt recognition is important.1 The patient presented with symptomatic severe bradycardia, a history of psychiatric disturbance, a slightly unusual body habitus and sexual development and abnormal ECG and echocardiographic findings, prompting a number of differential diagnoses before a unifying diagnosis was made, based on a revisited, detailed behavioural and eating history.
An 18-year-old Caucasian man presented to the acute cardiology service with a 6-month history of worsening breathlessness on exertion, increased fatigability, dizziness, generalised muscle aches and weight loss. From being an active football player, he found himself unable to play. Previous medical history included anxiety and autism spectrum disorder with input from mental health services and drug therapy with quetiapine. On examination, he was alert, tall and slim (body mass index (BMI) 16.75), with scant body hair and a bradycardia of 20 beats per minute. There was some hyperflexibility, but no muscle wasting or weakness, no neuropathy, no ataxia or tremor and normal reflexes and gait. On day 2 of admission, he developed a right sided Horner’s syndrome with no other physical findings.
The ECG showed a sinus bradycardia with episodes of sinus arrest and Wenckebach phenomenon (figure 1). Chest radiography was within normal limits. An echocardiogram showed mild right ventricular hypertrophy with apical dilatation and hypokinesis and a 17 mm pericardial effusion with no haemodynamic compromise. Full blood count revealed a white cell count of 2.7×109/L, neutrophils 0.8×109/L (1.7–6.5). Thyroid function tests, haematinics, extended liver function tests and urea and electrolytes were all within normal range. Immunological investigations were negative, including erythrocyte sedimentation rate (ESR), rheumatoid factor, anti-neutrophil cytoplasm antibodies (ANCA), antinuclear antibody (ANA) and monoclonal antibodies. Computed head tomography, magnetic resonance imaging of head and magnetic resonance angiogram detected no abnormalities and therefore ruled out stroke, carotid dissection or intracranial tumour as causes of his Horner’s syndrome. HIV, syphilis and hepatitis screens were negative. A pituitary profile was carried out revealing luteinizing hormone (LH) 0.6 IU/L (1.7–8.6), follicle stimulating hormone (FSH) of 1.0 IU/L (1.5–12), prolactin 191mIU/L (86 – 324), testosterone <0.4 nmol/L (8.6–29.0), sex hormone-binding globulin (SHBG) 95.4 nmol/L (18.3–54.1), cortisol 546 nmol/L, thyroid stimulating hormone (TSH) 1.9mIU/L (0.51–4.3), FT4 12.4 pmol/L (12.0–22.0), with normal MRI pituitary. Cardiac MRI confirmed global pericardial effusion, small bilateral pleural effusions, left ventricular ejection fraction of 57%, no myocardial oedema or myocardial scar and native T1 values within normal range.
The shortness of breath and fatigue were attributed to the profound bradycardia. The cause of this bradycardia was initially postulated to be secondary to quetiapine. However, withdrawal of this drug did not resolve the bradycardia. The normal levels of serum electrolytes eliminated hypokalaemia and hypomagnesaemia. The absence of neuropathy made hypovitaminosis B unlikely. Systemic inflammatory and autoimmune disorders were considered in view of the pericardial effusion, rhythm disturbance and breathlessness, shortness of breath, but eliminated by negative serology. Hypopituitarism was eliminated but there was evidence of hypogonadotrophic hypogonadism. Hypoalbuminaemia and mineral/vitamin deficiencies were ruled out as albumin, zinc, thiamine, copper, vitamin B6 and selenium were all within the normal range. Investigations noted above excluded carotid dissection, a space occupying lesion or apical lung pathology as a cause for the right sided Horner’s syndrome.
A conservative cardiac approach was adopted because there was slow improvement in the bradycardia and breathlessness. Testosterone treatment was initiated and quetiapine stopped. A unifying diagnosis was not established. After 9 days of observation and safe mobilisation in hospital, the patient was allowed home, with a plan for follow-up by specialists in cardiology, endocrinology, neurology and psychiatry.
Outcome and follow-up
During endocrine outpatient follow-up, it became apparent that the patient exhibited a restrictive eating pattern, eating small amounts only two times a day, following a strict gluten-free diet despite no history of coeliac disease, avoiding dairy products and drinking up to 8 L of water per day. He was also undertaking high levels of exercise, such as long nocturnal runs. Support from mental health services and dieticians resulted in a more balanced diet and pattern of activity. There was no distortion of body image or intent to lose weight therefore the symptoms were more consistent with that of avoidant/restrictive food intake disorder (ARFID) but no formal diagnosis is reported. Over the subsequent 6 months, the patient’s weight increased to a BMI of 18.5, the heart rate increased to 50−60 bpm, Horner’s syndrome resolved and fatiguability improved. A repeat echocardiogram revealed resolution of the pericardial effusion and good biventricular function.
This case demonstrates the cardiovascular, endocrine (and possibly neurological) consequences of an eating disorder, but under the care of the cardiology team, the diagnosis was not considered until after the patient was discharged, thus highlighting the importance of (sometimes sensitive) aspects of the personal history.
Eating disorders have well documented cardiovascular consequences; one study found up to 95% of patients presenting with bradycardia, with 70% having a heart rate below 50 bpm.1 Eating disorders carry the highest mortality rate of psychiatric conditions and this is thought to be attributable to an increased risk of sudden cardiac death from arrhythmia.2 Pericardial effusions occur less commonly but has been reported in >20% of patients.3 In cases in which the serum albumin is normal, the underlying pathophysiology is unclear, but resolution is usually observed with increased weight gain.4 Early recognition and a low threshold of suspicion are pivotal in adolescents presenting with symptoms attributable to the above with no obvious cause, such as in our case, which may have been an example of ARFID, which may be associated with an autistic tendency.5
Our case also demonstrates some of the consequences of an eating disorder on the endocrine system. Affected adolescent men have low BMI, testosterone and oestradiol levels. Endocrine dysregulation results in low gonadotrophin-releasing hormone (GRH) and LH, increased growth hormone and decreased insulin-like growth factor 1 (IGF1) levels. All of these features were demonstrated in our case, resulting in hypogonadotrophic hypogonadism.6 A recent case series described four male patients, all of whom demonstrated varying degrees of endocrine dysregulation and bradycardia.7
Our case posed diagnostic challenges because of the pathological bradycardia, abnormal appearance, pericardial and pleural effusions, unusual echocardiogram and endocrine dysfunction, with at first no unifying pathology. This was particularly difficult because the presentation was to a tertiary cardiology service unused to adolescents with an eating disorder. It would have been possible, and unfortunate, for instance, to commit a young person to insertion of a permanent pacemaker for a condition which subsequently turned out to be reversible. The eating disorder was unintentional and elucidating the details made challenging by autism. It was only a subsequent detailed personal history, taken by an endocrinologist and further reviewed by a gastroenterologist, that the true cause was revealed. This case highlights the importance of a sound and thorough history, even in these days of highly sophisticated investigations.
Presence of bradycardia in an adolescent with no obvious aetiology should prompt consideration of an underlying eating disorder.
Multidisciplinary input is often required to solve cases such as this and it may even require continued multidisciplinary follow-up before finding the answer.
When faced with a diagnostic challenge resulting in negative investigations, always return to the basics and ensure a thorough history is taken including social aspects.
The authors would like to acknowledge the contribution of the multispecialty team involved in the management and ongoing care of the patient in this case.
Contributors JG contributed to the diagnosis and management of the case, design and conceptualisation of the case report and review of the manuscript. EA contributed to design and conceptualisation of the case report, drafting and revision of manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.