Incidence and Causes of Disc Edema in Patients With Chronic Kidney Disease

Trial Information

Incidence and Causes of Disc Edema in Patients With Chronic Kidney Disease

The craniospinal cavity is enclosed by a rigid, non-compressible bone and thus has a
constant volume. It is filled with soft tissue (brain, spinal cord and connective tissue),
cerebrospinal fluid (CSF) and circulating blood. Intracranial pressure (ICP) is the pressure
of the fluid that bathes the brain and the spinal cord. The ICP is regulated by a fine
balance between the production and absorption of CSF. Any disturbance in the volumes of the
contents of the rigid craniospinal cavity will cause an alteration of the ICP. Intracranial
pressure can be elevated from a number of disease processes such as space occupying lesions,
abnormalities of the production and absorption of the CSF and abnormalities of the
circulation such as venous obstruction.

Raised ICP will symptomatically manifest as headache, vomiting, tinnitus and diplopia in
addition to neurologic symptoms related to the lesion location and type. The increased ICP
can be transmitted to the optic nerves causing papilledema, defined as swelling of the optic
nerve head (papilla) secondary to raised ICP. Swelling of the optic nerves in the absence of
raised ICP is termed disc edema (Parsons JH, Miller NR). Causes of disc edema are extensive
and include ischemic optic neuropathy, malignant hypertension, diabetic papillopathy,
uremia, intracranial hypotension (CSF leak).

Papilledema is considered a medical emergency and is investigated by means of neuroimaging
(to evaluate intracranial lesions) and lumbar puncture (to evaluate the opening pressure and
CSF contents). A diagnosis of Idiopathic Intracranial Hypertension (IIH) is made when there
is elevated ICP in the absence of clinical, laboratory or radiological evidence of any known
cause of raised ICP.

The most feared complication of untreated papilledema is progressive optic nerve atrophy
resulting in vision loss. Early recognition, investigation and treatment of papilledema and
its causes can prevent blindness.

Patients with chronic kidney diseases have a number of risk factors which predispose them to
the development of disc edema. Medical comorbidities such as hypertension and diabetes
mellitus increase their risk for optic nerve head diseases such as ischemic optic neuropathy
and diabetic papillopathy. Malignant hypertension, uremia and dialysis dysequilibrium
syndrome also are known to cause papilledema.

There are no studies in the English literature to date, on disc edema in patients with
kidney diseases. However, neuroophthalmologists have clinically observed that patients with
chronic kidney diseases appear to have an increased incidence of optic nerve swelling
(Corbett JJ, unpublished data). A study looking at optic nerve edema in this group of
patients is overdue and may determine additional guidelines in the management of patients
with chronic kidney diseases.

The patients enrolled in the study will undergo an optic nerve head examination by
ophthalmoscopy to identify patients with disc edema. If disc edema is detected on the
screening examination, the patients will be referred to the Neuroophthalmology service for
evaluation and investigations to determine the further management. The results of the
neuroophthalmologic workup for patients with disc edema will be reviewed to ascertain the
etiology of disc edema.