Neurocrit Care
https://doi.org/10.1007/s12028-019-00785-6

NEURO-IMAGES

Transcranial Doppler Monitoring
of Dialysis Disequilibrium in an ESRD Patient
with Traumatic Brain Injury
Shivani Ghoshal*, Jonathan Gomez and Aarti Sarwal
© 2019 Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society

Introduction
Dialysis disequilibrium syndrome (DDS) is a constellation of signs and symptoms including nausea, headache, seizures, encephalopathy, and even herniation and
death [1]. The syndrome is thought to originate from
osmolar shifts in dialysis leading to an acute increase in
brain water, cerebral edema, and reduced brain compliance [1–4]. End-stage renal disease (ESRD) patients with
new acute neurologic injury involving compromise of
the blood–brain barrier may be at particular risk of DDS
[4–6].
Here, we present transcranial Doppler (TCD) images
revealing marked intra-dialytic increased distal vascular resistance and compromised flow velocity in ESRD
patient with acute traumatic brain injury. Trends in
pulsatility indices during hemodialysis may be a useful
noninvasive bedside method to monitor for dialysis disequilibrium in ESRD patients with acute neurologic injury.
Case
A 73-year-old man with ESRD on hemodialysis for the
past 10 years, hypertension, and hyperlipidemia presented to the emergency department with headaches
after a fall 2 days prior to presentation. One day prior to
presentation, he did not tolerate his scheduled hemodialysis due to severe headache at the start of his dialysis.
On day of presentation, a computed tomography (CT)
scan of the head revealed 6-mm right cerebral convexity acute subdural hematoma and a hemorrhagic right
parietal parenchymal contusion with surrounding vasogenic edema (Fig. 1). There was associated mass effect
*Correspondence: sghoshal@wakehealth.edu
Department of Neurology, Wake Forest School of Medicine, Medical
Center Boulevard, Winston‑Salem, NC 27157, USA

on the right cerebral hemisphere with partial sulcal and
right lateral ventricle effacement, and 2–3-mm leftward
midline shift. CT angiogram of head and neck revealed
no significant carotid or intracranial vessel stenoses. The
patient was admitted to the neurointensive care unit
(neuro-ICU) for close neurologic monitoring and placed
on levetiracetam 500 mg twice daily for seizure prophylaxis. On arrival to the neuro-ICU, the patient was afebrile and hemodynamically stable with a blood pressure
of 161/41. He was awake, attentive, and fully oriented
with no focal deficits. Repeat CT head 6 h after the initial scan showed stable subdural hematoma. Hemodialysis was initiated to maintain his scheduled dialysis needs.
The dialysis was run without heparin, with dialysate
composition of sodium 140 mEq/L and blood flow rate
of 350 mL/min—identical to his outpatient prescription. Within first 3 h of hemodialysis, patient developed
progressive right-sided headache leading to nausea, and
vomiting and decrease in level of consciousness. He had
no changes in mean arterial pressure during his hemodialysis. He intermittently opened eyes to stimulation but
required persistent painful stimulation in order to stay
awake with orientation to name and location only. He
developed focal weakness with following commands on
the right side but withdrawal to pain on the left on painful stimuli only. Hemodialysis was interrupted for an
emergent CT head, which revealed stable right cerebral
convexity subdural hematoma, with no interval change in
right parietal hemorrhagic contusions and surrounding
vasogenic edema. His serum BUN had decreased from 80
to 43 mg/dL, and his serum sodium remained unchanged
at 140 mEq/L.
The patient was being monitored by real-time TCD
with continuous waveform during his hemodialysis to
monitor cerebral hemodynamics as a part of a research

Fig. 1 Admission CT head, images at levels of lateral ventricles and midbrain. a 6-mm acute subdural hematoma along right cerebral convexity
with slight mass effect onto right lateral ventricle. b Acute subdural hematoma with no effacement of brainstem ambient cisterns. c High right
parietal IPH with minimal surrounding vasogenic edema

Fig. 2 Left and right MCA TCD waveforms during dialysis, shown on the left and right, respectively. a Baseline immediately prior to dialysis, b dialy‑
sis hour 1, c dialysis hour 2, and d dialysis hour 3. MFV is reported as the first value on the left upper corner, PI is reported as the third value in the
left upper corner. Through dialysis, velocities and waveforms on the left MCA stay relatively unchanged, with a slight increase in pulsatility index. On
the right MCA, velocities are progressively reduced through dialysis, with markedly increased pulsatility index (marked by red rectangle) indicating
increased distal resistance to flow (Color figure online)

Pulsa lity index (PI)

MCA PI CHANGES DURING DIALYSIS

4
3
2
1
0

0

1

2

3

HOURS OF DIALYSIS

Axis Title

Mean flow velocity
(MFV, cm/s)

(A)

RIGHT MCA PI

80
60
40
20
0

LEFT MCA PI

MCA MFV CHANGES DURING DIALYSIS

0

1

2

3

HOURS OF DIALYSIS

Axis Title

(B)

RIGHT MCA MFV

LEFT MCA MFV

Fig. 3 Patient MCA MFV and PI trends during dialysis. a MCA PI
trends during dialysis. b MCA MFV trends during dialysis

investigation (Fig. 2a–d). Through his dialysis, the
patient developed progressively increased distal resistance to flow, measured by pulsatility index (PI) at his
bilateral middle cerebral arteries (MCA) with a decrease
in MCA velocities. This change was particularly notable
on the right side, the same side as his subdural hemorrhage and cerebral contusions (Fig. 3a, b). Hemodialysis
was stopped, with minimal improvement in the patient’s
examination. Due to his persistently poor level of consciousness, electroencephalogram continuous monitoring was connected and showed development of
non-convulsive status epilepticus 6 h later.

Discussion
During hemodialysis, urea and other toxic solutes are
transported from blood into the dialysate solution, and
ultrafiltration removes excess body water. Patients with
chronic uremia may have both reduced expression of
brain urea transporters and increased expression of
aquaporin transporters. Urea’s poor reflection coefficient
can lead to an increased brain–plasma osmolal gradient,
causing the increased brain water content in hemodialysis seen on neuroimaging studies [2, 3].
In ESRD patients with an acute neurologic injury,
impaired blood brain barrier and decreased cerebral
compliance further complicate the effect of intra-dialytic fluid shifts [5]. Rapid correction of serum BUN and
high flow rates are thought to be potentiating factors
for dialysis disequilibrium in these patients due to their

compromised blood brain barrier [6]. Though detection
of dialysis disequilibrium typically relies on neurologic
examination changes and radiographic evidence of cerebral edema, these approaches are limited by their static
or post hoc nature [4, 5].
TCD ultrasonography is a reproducible, noninvasive
bedside measurement to assess cerebral hemodynamic
changes in mean flow velocity (MFV) and distal vascular
resistance (or PI) [7]. PI was calculated in this patient’s
case by subtracting end diastolic velocity from peak systolic velocity and dividing the value by MFV. Though
the utility of TCD has been established in patients
with intracranial atherosclerosis, subarachnoid hemorrhage, traumatic brain injury, and brain death, TCD
has not yet been used as a method of detecting dialysis
disequilibrium.
Our patient did not show substantial risk for midline
shift, mass effect, or herniation radiographically prior
to dialysis (Fig. 1). His subdural was relatively small,
with minimal mass effect on the right lateral ventricle
and no effacement of brainstem ambient cisterns. He
had no previous history of dialysis disequilibrium in his
past 10 years of dialysis. His imaging studies were stable over 24 h prior to dialysis. Continuous veno-venous
hemofiltration (CVVH) was not considered for this
patient due to his long-standing stability on hemodialysis, small subdural, and minimal neurologic deficits. His
neurologic examination on admission did not show any
focal neurologic deficits, but these are developed during dialysis with hemodynamic correlates on increased
distal resistance and impaired MCA velocities. The
rapid decrease in BUN and high flow rate during dialysis may have potentiated disequilibrium syndrome
leading to increased cellular edema and ischemic deficits on right side of brain. TCD monitoring showed
increased PI and decreased MFV through hemodialysis
prior to the patient’s sudden change in mental status at
hour 3 of treatment. His eventual development of nonconvulsive status epilepticus may have arisen from his
increased vascular resistance and compromised flow
causing a pro-epileptic cerebral metabolic crisis.
It is difficult to predict the degree of brain water
increase during hemodialysis. ESRD patients with acute
brain injury may be at particular risk of dialysis disequilibrium syndrome. It is possible continuous slow
dialysis forms such as CVVH may be more protective
against secondary neurologic injury in these high risk
patients. Currently, there are no bedside measures to
guide either dialysis modality choice or when to transition from continuous to intermittent hemodialysis in
acutely brain-injured ESRD patients requiring dialysis.
Here, we show TCD ultrasonography in ESRD patients
in the neuro-ICU as a novel, practical application of

bedside imaging to identify dialysis disequilibrium in
our patient. TCD may be a useful application of bedside
imaging to identify cerebrovascular changes potentially
associated with dialysis disequilibrium.
Author Contributions
All authors contributed equally to the production of this manuscript.
Source of support
None.
Conflicts of interest
Authors Ghoshal, Gomez, and Sarwal have no conflicts of interest.
Ethical Approval/Informed Consent
These data were obtained by IRB approval and informed consent, with adher‑
ence to ethical guidelines.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in pub‑
lished maps and institutional affiliations.

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