NDT Advance Access originally published online on January 12, 2007
Nephrology Dialysis Transplantation 2007 22(3):945-948; doi:10.1093/ndt/gfl726
© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
(Section Editor: A. Meyrier)
From the heart to the soul
Polycarpos Polycarpou1,
Efthyvoulos Anastassiades2 and
Loizos Antoniades3
1Department of Nephrology, Timios Stavros Hospital, Larnaca, 2Department of Nephrology, Aretaeion Hospital, Nicosia and 3Department of Cardiology, Nicosia General Hospital, Cyprus
Correspondence and offprint requests to: Polycarpos Polycarpou, Email: drpolys{at}cytanet.com.cy
Keywords: culture negative; delirium; haemodialysis; infective endocarditis; transoesophageal echocardiogram
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Introduction
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Delirium is defined as a transient global impairment of cognition.
It is associated with increased morbidity and mortality. There
is a variety of clinical conditions that can produce delirium
in the general population (
Table 1). Delirium may be the only
presenting symptom of a serious underlying disease, especially
in patients on dialysis and in the elderly.
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Case report
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A previously fit, 78-year-old retired farmer established on
haemodialysis for 5 years, presented with anorexia and severely
altered mental state, singing ecclesiastical hymns all day long.
Clinical examination revealed only the presence of an already
known pansystolic murmur at the mitral area. He was not on any
medication that could be implicated in causing acute confusion,
he had never been treated with aluminium-containing phosphate
binders in the past and his wife confirmed that he had not ingested
star fruit or unusual mushrooms recently. His white cell count
was 12 000 (89% neutrophils), Hb 9.8 g/dl with normal mean corpsular
volume (MCV), erythrocyte sedimentation rate (ESR) 98 and C-reactive
protein(CRP) 15 mg/dl. Full biochemistry, arterial blood gases,
three sets of blood cultures, urine culture, chest x-ray, thyroid
function tests, Treponema Pallidum Haemaglutination Assay and
CT head were all normal.
His disturbed psychological and mental state was gradually deteriorating with intense ideas of persecution. He was refusing food and was continuously murmuring incomprehensible religious hymns. There was no pyrexia [Pyrexia = Fever (origin greek ‘pyr’ meaning fire, pyrexial = somebody ‘who is on fire’)] or other new clinical signs but he had persistently raised ESR and CRP, suggesting an organic cause for his symptoms. A repeat full septic screen (including a lumbar puncture with India Ink staining for cryptococci), clotting, Vit B12 levels, virology and vasculitis screen, Brucella and Chlamydia titres and bone marrow aspiration for tuberculosis were all negative. There was, however, a strongly positive rheumatoid factor (RF). Within the next few days the patient's clinical condition deteriorated significantly to the extent that he was unable to communicate with his environment. Examination was again unremarkable with no focal neurology and no pyrexia.
Because of the combination of positive RF and CRP, repeat blood cultures were taken with the request to be incubated for 7 days for the HACEK group of bacteria (Haemophilous, Actinobacillus, Cardiobacterium, Eikenella and Kingella), known to be involved in infective endocarditis. A transoesophageal echocardiogram was requested but, due to a long waiting list, a trans-thoracic Echocardiogram was first performed by the cardiology team which was reported as showing mild/moderate mitral regurgitation but no vegetations. The patient's condition deteriorated even more to the extent that we were contemplating the cancellation of his transoesophageal echocardiogram when he was called for it, as he was so ill. The latter, however, revealed the presence of severe mitral regurgitation with a posterior leaflet vegetation. He was started on benzyl penicillin, gentamicin and vancomycin. Within 48 h his general condition improved. Seven days into treatment he was back to normal, eating and drinking. His blood cultures remained negative. He continued antibiotics for a total of 6 weeks and now continues on haemodialysis thrice weekly and occasionally sings the odd ecclesiastical hymn as a reminder to us all of his near-fatal episode.
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Discussion
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Delirium is a syndrome caused by various diseases that result
in similar symptoms. The word delirium is derived from the latin
word delirare which means ‘to be silly’, ‘be
off the tract’. The condition has been described by Hippocrates
himself. The pathophysiology of delirium is not very well understood.
The fact that there are so many different aetiologies that can
cause delirium (
Table 1), renders it unlikely that a single
mechanism is operative. A systemic organized approach is required
to try to identify the underlying cause. Medicine toxicity is
responsible for about 30% of all cases of delirium [
1]. Thus,
the most important initial step is a medication review. The
most common suspects are listed in
Table 2. The evaluation of
delirium in the dialysis patient is generally the same as in
the non-dialysis patient. However, the nephrologist must also
consider some causes of delirium that occur exclusively in the
dialysis patient and these are outlined in
Table 3. Patients
on dialysis are susceptible to a variety of uncommon insults
that can cause delirium such as minor head injuries resulting
in subdural haematomata (in a group of patients that regularly
receive anticoagulation), unusual infections (e.g. cryptococcal
meningitis) and drug intoxication (due to impaired renal clearance).
In our case, the raised inflammatory markers, suggested to us
that we had to exclude an underlying inflammatory condition
and the combination of raised CRP and positive RF prompted us
to look hard for infective endocarditis (IE).
Compared with the general population, IE occurs much more commonly
and has far worse outcome in the chronic dialysis patients,
with one-year mortality in the range of 40–60% [
2,
3].
IE was first described by Osler in 1885. The pattern of the
disease has changed considerably since the introduction of antibiotics.
Mitral valve prolapse and degenerative valve disease (including
calcific valve disease in dialysis patients) have replaced rheumatic
heart disease as the most common predisposing conditions. The
predominant organisms causing IE in this group of patients are
Gram-positive bacteria (mainly due to vascular access related
bacteraemia) [
2,
4,
5,
12]. The diagnosis of IE itself remains
a challenge to physicians as it often has an uncharacteristic
presentation. The full house of classical signs with changing
heart murmur, splinter haemorrhages, Osler's nodes etc., is
very rarely found. In elderly patients and in chronic renal
failure the presentation may be even more atypical. In this
group of patients, the pyrexial response is often blunted and
constitutional symptoms of weight loss, anorexia and malaise
are often the prominent ones. Relatives may seek medical advice
because the patient has become confused, disorientated, or because
he/she has developed psychiatric symptoms as was the case with
our patient. A number of studies have shown that neurological
complications including meningitis, toxic confusion, major thromboembolic
phenomena, headache and neuropsychiatric manifestations including
psychosis can occur in up to 20–30% of IE cases [
6]. The
combination of positive CRP and positive RF is suggestive of
IE with a positive predictive value (for positive RF) 91.3%
[
7]. Blood culture remains the most important laboratory test
and yields the causative micro-organism in >80% of the patients.
About 10–20% of cases of endocarditis will fail to show
a positive blood culture [
8] and this is commoner in conditions
of impaired immune response [
9], such as chronic renal failure.
Usual causes of culture-negative endocarditis are previous recent
treatment with antibiotics, fastidious organisms (e.g. HACEK),
intracellular pathogens (e.g. Chlamydia, Coxiella), fungal infections
and renal failure itself [
9,
10]. In addition to blood cultures,
transoesophageal echocardiography is the most useful diagnostic
examination for IE in these patients [
2,
11].
As Doulton has pointed out ‘... every effort should be made to avoid ectopic valvular calcification in the haemodialysis patients as this approach can potentially reduce the risk of developing IE’ [4]. Antibiotic prophylaxis against IE has been suggested for all dialysis patients, but this strategy is controversial and unproven [2].
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Teaching points
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- Almost any medical illness can cause delirium. Patients with delirium are ill. However, patients on dialysis with delirium may not look ill apart from their behavioural change. Patients with infections may present without fever, patients with intracranial haemorrhage may present without localising signs, patients with meningitis may present without neck stiffness.
- IE occurs much more commonly in the haemodialysis patients, mainly via vascular access related bacteraemia. If there is strong clinical suspicion of the disease, a transoesophageal echocardiogram should be requested even in the presence of negative blood cultures.
- Transoesophageal echocardiogram should not be forgotten in the evaluation of neuropsychiatric conditions.
Conflict of interest statement. None declared.
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References
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- Francis J. (1996) Drug-induced delirium: diagnosis and treatment. CNS Drugs 5:103.
- Ireland JH and Mc Carthy JT. (2003) Infective endocarditis in patients with kidney failure: chronic dialysis and kidney transplant. Curr Infect Dis Rep 5:293–299.[Medline]
- Walpot J, Blok W, van Zwienen J, Klazen C, Amsel B. (2006) Incidence and complication rate of infective endocarditis in the Dutch region of Walcheren: a 3-year retrospective study. Acta Cardiol 61:175–181.[CrossRef][Web of Science][Medline]
- Doulton T, Sabhharwal N, Cairns HS, et al. (2003) Infective endocarditis in dialysis patients: new challenges and old. Kidney Int 64:720–727.[CrossRef][Web of Science][Medline]
- Spies C, Madison JR, Schatz IJ. (2004) Infective endocarditis in patients with end-stage renal disease: clinical presentation and outcome. Arch Intern Med 164:71–75.[Abstract/Free Full Text]
- Bademosi O, Falase AO, Jaiyesimi F, Bademosi A. (1976) J Neuropsychiatric manifestations of infective endocarditis: a study of 95 patients. Neurol Neurosurg Psychiatry 39:325–329.
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- Werner M, Anderson R, Olaison L, Hokevik L. (2003) Clinical study of culture-negative endocarditis. Medicine (Baltimore) 82:263–73.[CrossRef][Medline]
- Oakley CM. (1995) The medical treatment of culture-negative infective endocarditis. Eur Heart J (Review) 16:Suppl B, 90–93.
- Houpikian P and Raoult D. (2005) Blood culture negative endocarditis in a reference centre: etiologic diagnosis of 348 cases. Medicine(Baltimore) 84:162–173.[CrossRef][Medline]
- Horstkotte D and Piper C. (2004) New aspects of infective endocarditis. Minerva Cardioangiol (Review) 52:273–286.
- Manian FA. (2003) Vascular and cardiac infections in end-stage renal disease. Am J Med Sci (Review) 325:243–250.[CrossRef]
- Drug induced delirium: diagnosis, management and prevention. Drug & therapy perspectives (ISSN: 1172-0360). (1997) 10:5–9.
- Schmidt RJ and Holley JL. (2006) Psychiatric illness in dialysis patients. In Rose BD (Ed.). UpToDate, Wellesley, MA.
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Introduction
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