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Received for publication: 6.11.09; Accepted in revised form: 7.1.10
Nephrol Dial Transplant (2010) 25: 22722275
doi: 10.1093/ndt/gfq013
Advance Access publication 26 January 2010
High but stable incidence of subdural haematoma in haemodialysisa
single-centre study
Albert Power, Mohamed Hamady, Seema Singh, Damien Ashby, David Taube and Neill Duncan
West London Renal and Transplant Centre, Hammersmith Hospital, Imperial College Healthcare NHS Trust, DuCane Road, London
W12 0HS, UK
Correspondence and offprint requests to: Albert Power; E-mail: albert.power@imperial.nhs.uk
Abstract
Background. The incidence of subdural haematoma
(SDH) is high in haemodialysis (HD), with data suggesting
an increasing incidence over time. The prognosis remains
poor with 40% mortality at 30 days. The extent of this
problem in non-US populations has not been described
in the literature.
Methods. We conducted a retrospective, single-centre UK
study of non-traumatic SDH in patients established on
maintenance HD between 1 January 2002 and 1 June 2009.
Results. The prevalence of SDH was 0.4% at our centre
with an overall annual incidence of 189 per 100 000 pa-
tients. SDH was associated with increased patient age
(mean 71.3 8.5 years) but not associated with a higher
prevalence of major comorbid conditions and antiplatelet
or anticoagulant use. Mortality was high (46% at 30 days,
58% at 1 year). We did not observe a trend to increasing
prevalence of this condition over time.
Conclusions. SDH has a higher (>20 times) incidence in
HD patients than in the general population and is associat-
ed with high mortality. Although the prevalence in this
study was lower than in published US studies, the inci-
dence rate is similar. Further studies to validate prognostic
criteria that guide decisions regarding surgery are required.
Keywords: haemodialysis; haematoma evacuation; subdural haematoma
Introduction
The incidence of stroke in patients on maintenance haemo-
dialysis (HD) is 510 times that of the general population,
with a higher prevalence of haemorrhagic events [13].
Studies evaluating stroke in this patient population have
traditionally excluded subdural haemorrhage (SDH) from
analyses. There are just two studies of SDH in dialysis pa-
tients to date in the literature both deriving from US popu-
lations [4,5]. The incidence of SDH in dialysis patients is
higher than in the general population, with a mortality
reaching 40% [5]. One study suggested that the incidence
of SDH was stable in patients on peritoneal dialysis but
steadily increasing among HD patients [5]. There are no
European studies to guide management and no studies
have reported exclusively on a HD population during the
last decade. We studied the incidence of non-traumatic
SDH in maintenance HD patients at our centre and exam-
ined the demographics and clinical characteristics of pa-
tients who developed SDH.
Subjects and methods
The West London Renal and Transplant Centre (comprising of the renal
units of Hammersmith, St. Marys and Charing Cross Hospitals) provides
renal services to a population of over 2 million people and cares for a total of
1200 HD patients who receive their treatment in 10 satellite dialysis units.
This retrospective study identified all patients established on mainte-
nance HD (defined as receiving >90 days continuous treatment) from 1
January 2002 to 31 May 2009 at St. Marys Hospital (January 2002
September 2005) and the West London Renal and Transplant Centre at
Hammersmith Hospital, London (October 2005May 2009). All paper
and electronic records from both sites relating to admission, inpatient stay,
laboratory tests, radiological investigations and inpatient and outpatient
dialysis data were analysed. Non-traumatic SDH was defined in accor-
dance with the International Classifications of Diseases, Ninth Revision
criteria (Code 432.1). All cases of SDH were reviewed by the neurosurgi-
cal team at our centre with regards to surgical treatment.
Patients were dialysed three times weekly using low-flux synthetic AM-
BIO-1000Wet (Asahi Kasei Medical Europe GmbH, Frankfurt, Germany)
and Nipro Sureflux-L (Nipro Europe NV, Zaventem, Belgium) haemodia-
The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
For Permissions, please e-mail: journals.permissions@oxfordjournals.org
2272 A. Power et al.

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lysers during the periods 2002January 2009 and FebruaryMay 2009,
respectively. Unfractionated heparin (Monoparin sodium heparin, CP
Pharmaceuticals, Wrexham, UK) was used for dialysis circuit anticoagu-
lation apart from the period September 2008January 2009 where tinza-
parin (Innohep, Leo Pharma, Princes Riseborough, UK) was at an initial
dose of 2500 U at the start of dialysis as previously described [6]. Unfrac-
tionated heparin was administered as a 500-IU bolus at the start of dialysis
followed by a maintenance dose of 500 IU/h thereafter. Patients weighing
in excess of 80 kg received an increase in the bolus and maintenance dose
of 50 IU/kg excess weight. Dialysis session length varied from 4 to 5 h.
Dialysis adequacy was measured by single-pool Kt/V (spKt/V) using the
Daugirdas method on a monthly basis [7]. Dialysis prescription was tai-
lored to achieve a spKt/Vof 1.6.
Statistics
Descriptive statistics are expressed as the mean standard deviation.
Continuous and categorical variables were compared using Students t-test
and the chi-square or MannWhitney U-test, respectively, as appropriate.
Timeline incidence data were analysed using a Poisson model and ex-
pressed with 95% confidence intervals (CI). Statistical significance was
defined by P < 0.05. STATISTICA 9.0 (StatSoft Inc., Tulsa, OK, USA)
was used to perform the statistical analysis.
Results
During the study period, a total of 2542 patients received
maintenance HD. Complete demographic, clinical and
therapeutic data was available in 2155 patients comprising
the study cohort with a total of 7508 patient-years follow-
up. Population demographics are presented in Table 1.
Eleven patients (0.4% cohort) experienced non-traumatic
SDH (mean patient age of 71.3 8.5 years, mean time on
HD of 2.8 2.3 years, mean spKt/Vof 1.72 0.29); 5/11
(45%) patients were diabetic, 6/11 (55%) hypertensive and
1/11 (9%) had established cerebrovascular disease (past
transient ischaemic attacks and/or stroke). There was no
significant association between SDH occurrence and anti-
platelet or anticoagulant use. The presence of diabetes, hy-
pertension or cerebrovascular, coronary or peripheral
vascular disease was not significantly associated with
SDH (Table 2). There was no evidence of derangement
of haematological parameters at the time of SDH (Table 3).
The overall annual incidence rate of SDH was 188.6 per
100 000 patients per year in our population (95% CI 97.5
329.5). This is similar to the recent (2002) rate of 191
per 100 000 patients per year reported in a recent study
based on USRDS data, but in contrast, there was no ev-
idence of an increasing incidence rate over time (Figure 1)
[5]. Patient mortality was 46% at 30 days and 58% at 1
year. Subdural thickness was >20 mm in 7/11 (64%) cases
and there was a significant (>10 mm) associated midline
shift in 4/11 (36%) cases. The majority (86%) of patient
deaths occurred in patients deemed not fit for operative
treatment with SDH thickness >20 mm and/or midline shift
>10 mm. All these patients died directly as a result of SDH.
Discussion
SDH develop from bleeding into the space between the du-
ra and the arachnoid membranes and are seen most com-
monly following head trauma. Acute SDH occur following
traumatic shear force, tearing the bridging veins on the sur-
face of the brain in the majority of cases with around 25%
attributed to arterial rupture [8]. Traction injury to venous
structures from low cerebrospinal fluid (CSF) pressure,
Table 1. Demographic characteristics of the study cohort (2002June
2009)
Mean age (years) 57.9 16.1
Ethnicity
White 905 (42%)
Afro-Caribbean 409 (19%)
South Asian 733 (34%)
Other 108 (5%)
Comorbidities
Diabetes 829 (38%)
Ischaemic heart disease 686 (32%)
Hypertension 1202 (56%)
Peripheral vascular disease 247 (12%)
Cerebrovascular disease 327 (15%)
Therapies
Aspirin 823 (38%)
Clopidogrel 226 (11%)
Warfarin 61 (3%)
Table 2. Comparative demographic characteristics of patients with and
without SDH
SDH present No SDH present P-value
Mean patient age (years) 71.3 8.5 57.9 16.1 0.006
Mean time on HD (years) 2.8 2.3 3.5 3.5 0.5
Diabetes 5 (46%) 829 (38%) 0.6
Ischaemic heart disease 4 (36%) 686 (32%) 0.7
Hypertension 6 (55%) 1202 (56%) 0.5
Peripheral vascular disease 1 (9%) 247 (12%) 0.9
Cerebrovascular disease 1 (9%) 327 (15%) 0.3
Aspirin 6 (55%) 823 (38%) 0.3
Clopidogrel 0 226 (11%) 0.3
Warfarin 0 61 (3%) 0.7
Data are expressed as mean standard deviation and patient number and
percentage in parentheses.
Table 3. Haematological parameters at time of SDH
Mean haemoglobin (g/dl) 12.0 2.3
Mean platelet count (10
9
/ml) 183 73
Mean PT (s) 11.7 0.9
Mean APTT (s) 30.4 3.5
Mean fibrinogen (g/L) 4.11 0.79
PT, prothrombin time; APTT, activated partial thromboplastin time.
0.0
50.0
100.0
150.0
200.0
250.0
300.0
350.0
400.0
1 2 3 4 5 6 7 8
Year
S
D
H

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1
0
0
,
0
0
0

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s

p
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e
a
r
Fig. 1. Annual incidence rate of SDH during the period of study.
Subdural haematoma in haemodialysis 2273

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typically as a result of spontaneous or iatrogenic CSF leak-
age (such as following diagnostic lumbar puncture), has al-
so been implicated in the pathogenesis of SDH. Significant
cerebral atrophy, a finding that increases in prevalence with
advancing age, and the use of antithrombotic agents are
major risk factors for SDH [9]. In addition, SDH has been
described in association with subarachnoid haemorrhage,
arteriovenous malformations and meningiomas [1012].
HD is associated with fluctuations in cerebral blood
flow and an increase in intracranial pressure [13,14]. By
contrast, there is a reduction in the pressure within the
SDH cavity intradialytically [15]. The bleeding diathesis
of uraemia is exacerbated by the use of anticoagulants such
as heparins and coumarins in dialysis circuit anticoagula-
tion, vascular access patency and management of atrial fi-
brillation [16,17]. This is compounded by the use of
antiplatelet agents for coronary and peripheral arterial dis-
ease in an ageing HD population with a high prevalence of
cerebrovascular disease and cerebral atrophy [18,19]. It
can be hypothesized that the mechanical forces described
above may trigger non-traumatic SDH formation in pa-
tients at high risk for this lesion.
The incidence of non-traumatic SDH in HD patients in
this study is more than 20 times that in the general popu-
lation (38/100 000 patients per year) [20,21], with an
overall incidence rate that is similar to that in the US.
The prevalence of SDH in our HD population was much
lower than previously reported (0.4 vs 3%) [4]. This is like-
ly to be multifactorial and may reflect differences in patient
demographics, dialysis circuit technology and anticoagula-
tion and use of oral anticoagulants. We do not use warfarin
for vascular access patency and have a low prevalence of
arteriovenous graft (AVG) use (1% prevalent population
currently). As the authors point out, the increasing inci-
dence of SDH in the US may relate to an increase in
AVG and consequent warfarin use [5].
In keeping with studies from the general and HD popu-
lation, it is associated with increasing age where it carries a
poor prognosis [2022]. Patients with SDH in this study
were significantly older than controls73% were >65
years old. This is similar to available US data [5]. We
did not observe an over-representation of major comorbid
conditions in patients with SDH in this study, in contrast to
prior published work [5]. This may reflect a different ethnic
case mix to that reported in US studies, with a lower per-
centage of African-American patients and a greater propor-
tion of South Asians in UK studies, but can also be
influenced by the considerably smaller number of affected
patients in this study. We did not observe an association
with antiplatelet agent or warfarin use, although this could
be subject to prescription bias (i.e. elderly patients consid-
ered at high risk of falls are less likely to be prescribed po-
tent anticoagulation) and bias by indication. The recorded
absence of preceding head trauma could have been subject
to reporting bias from the patient and/or their carers who,
in addition, may not have reported minor trauma that has
been implicated in SDH pathogenesis [23]. The retrospec-
tive nature of this study cannot demonstrate causation.
Patient mortality was high (46% at 30 days) and sim-
ilar to US data [5]. No recent study in HD patients to
date has comprehensively examined clinical outcomes
following diagnosis. An initial study by Leonard et al.,
reporting on 13 patients, found poor survival (15%)
and surgical outcomes [4]. There are no rigorous, pub-
lished studies on clinical outcomes in HD patients with
SDH whether managed conservatively or surgically. Data
from the general population suggest a worse prognosis
with a lower Glasgow Coma Scale score (GCS) [24],
greater haematoma thickness [25] and the degree of mid-
line shift [22,26]. These clinical and radiological criteria
have not been validated in HD patients. Available surgical
guidelines recommend surgical evacuation for patients
with an acute SDH and who have a haematoma thickness
>10 mm or midline shift >5 mm regardless of the level of
the GCS [27]. Our study suggests that similar criteria
may be appropriate in this patient population but the results
need to be approached with caution. Appraisal of fitness for
surgery was potentially influenced by the appreciation of
the natural bleeding diathesis [28] and the comorbid burden
of HD patients. In total, 3/11 (27%) patients proceeded to
surgery as determined by clinical and neuroimaging criteria
described above. No patients died in the immediate post-
operative period (one patient died after 43 days, the other
after 355 days).
Tailored and judicious anticoagulation, avoidance of po-
tentially pathogenic circulatory volume shifts on HD and
blood pressure control may all have a role to play in reduc-
ing the incidence of SDH in the HD population. There is a
paucity of data on the epidemiology of SDH in Europe.
Published data from the US give grounds for concern but
describe different populations and HD practices to those in
Europe [2933]. We believe that larger global studies are
required to determine the incidence, prevalence and prog-
nostic impact of SDH. In addition, prospective validation
of established criteria for surgical intervention need to be
undertaken in this high-risk group with potential to im-
prove short-term and long-term outcomes.
Conflicts of interest statement. None declared.
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Received for publication: 11.12.09; Accepted in revised form: 7.1.10
Nephrol Dial Transplant (2010) 25: 22752283
doi: 10.1093/ndt/gfp781
Advance Access publication 26 January 2010
Perioperative outcomes among patients with end-stage renal disease
following coronary artery bypass surgery in the USA
Dipen S. Parikh
1,2,3
, Madhav Swaminathan
4
, Laura E. Archer
5
, Jula K. Inrig
1,2,6
, Lynda A. Szczech
1,2
,
Andrew D. Shaw
4
and Uptal D. Patel
1,2
1
Division of Nephrology, Department of Medicine, Duke University Medical Center, Durham, NC, USA,
2
Duke Clinical Research
Institute, Duke University Medical Center, Durham, NC, USA,
3
Vascular Access Center of Durham, Durham, NC, USA,
4
Division of
Cardiothoracic Anesthesiology, Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA,
5
Division of
Biostatistics, Duke Comprehensive Cancer Center, Duke University Medical Center, Durham, NC, USA and
6
Division of Nephrology,
Department of Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA
Correspondence and offprint requests to: Dipen S. Parikh; E-mail: dipenparikh@yahoo.com
Abstract
Background. Patients with end-stage renal disease (ESRD)
requiring chronic haemodialysis who undergo coronary ar-
tery bypass graft surgery (CABG) are at significant risk for
perioperative mortality. However, the impact of changes in
ESRD patient volume and characteristics over time on op-
erative outcomes is unclear.
The Author 2010. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Outcomes among ESRD after CABG 2275

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