DISCUSSION
There are many etiologies that have been known to cause seizures. These
include epilepsy, hemorrhagic stroke, cerebral hypoxia, metabolic
derangement, thyroid disease, head trauma, CNS infection, vascular
malformations, intoxication, poisoning and some of the rarer causes
include brain tumors, hypertensive encephalopathy or
PRES.6
Our patient had an extensive seizure work up during his hospital
admissions. One of the most important tests to perform is VEEG as this
provides insight as to the type of seizure a patient may be having and
if there is underlying epilepsy.7,8 Continuous VEEG
was performed on our patient during both admissions for seizures.
Obtaining continuous VEEG monitoring or at least four separate VEEGs
increases the chance of picking up underlying epileptic pathology by
about 80-90%.9,10 Continuous VEEG in our patient
never identified any wave-forms suggestive of epilepsy. Neuroimaging is
another crucial component of the seizure work up. Typically brain
magnetic resonance imaging (MRI) is preferred over CT scan as MRI has
higher sensitivity for epileptogenic lesions as well as having superior
soft tissue contrast for identifying any other possible underlying
pathology, but CT scans are often sufficient enough to make an accurate
diagnosis.7,11,12 Our patient had CT scans of the
brain on both presentations but showed no abnormality suggesting the
cause of his seizures. In this patient CT scans of the brain were
preferred over MRI originally given the patient acuity as CT scans can
be obtained quicker than an MRI and are often sufficient in identifying
any potential causes of seizures.7,8,13 Typically
seizure work up can be continued with outpatient MRI; however, in our
case it was deferred as CT brain and VEEG were normal and an MRI was not
going to change our treatment plan especially since the patient did not
have any additional seizures once his blood pressure was controlled.
Additional work up of seizures includes blood work to evaluate metabolic
and thyroid issues and ECG and lumbar puncture to rule out hypoxic
cerebral injury from syncope and infectious processes
respectively.7,14,15 Although there were some
abnormalities in his lab results there was nothing evident as the cause
of his seizures (Table 1). ECGs were done on our patient and were
insignificant. Moreover, since there were no infectious signs or
symptoms and blood cultures never showed any growth of organisms, a
lumbar puncture was not indicated.
Given the extensive negative neurologic, hematologic, and infectious
workup, seizures in our patient likely occurred due to hypertensive
encephalopathy from increased intracranial pressure. The cerebral
perfusion pressure (CPP) of the brain has a narrow and sensitive window
that is easily affected by changes in systemic BP. Normally when there
is an increase in systemic BP the cerebral vasculature vasoconstricts to
maintain CPP in physiologic range. In sudden increases of systemic BP or
uncontrolled hypertension CPP is not maintained and can lead to cerebral
edema resulting in neurologic dysfunction manifesting as
seizures.16,17 After our patient’s blood pressure was
stabilized during admission, he did not have any additional seizures
suggesting that the cause of his seizures was severely elevated blood
pressures.
Acute or chronic kidney disease have been shown to cause hypertensive
emergency and encephalopathy.4,5 80-85% of patients
with chronic kidney disease (CKD) have hypertension.18Hypervolemia is due to decreased glomerular filtration rate (GFR), which
results in sodium retention and extracellular fluid
expansion.19 Furthermore, an overactive
renin-angiotensin system due to renal ischemia can lead to increased
angiotensin II and renin causing increased systemic BP, while uremia and
decreased renal clearance can cause a neural reflex that increase levels
of the vasoconstrictor endothelin.20 Some of the
implicated renal diseases that can follow this physiology include acute
glomerulonephritis, renal vascular disease, renal infarction, and renal
failure. Anti-GBM disease is a rapidly progressive glomerulonephritis
falling under this category.
Regarding treatment, initial management of this patient was aimed at
controlling the seizure. Patients experiencing seizures without a
history of epilepsy are typically treated with a single antiepileptic
medication.21 Our patient received lorazepam to
terminate the seizure and levetiracetam to prevent recurrence of
seizures. Typically, anti-epileptic medications are not required for
acute seizure management as seizures resolve on their own within a few
minutes unless the patient is critically ill or has underlying metabolic
derangements.22 Given that our patient was critically
ill with renal disease and a dangerously elevated BP on presentation,
levetiracetam was given to prevent further seizures, which has been
shown to be more effective and have more long term benefits compared to
other prophylactic seizure medications.16
Controlling BP in hypertensive emergency with hypertensive
encephalopathy and ESRD varies by physician preference, although most of
the treatments focus around IV antihypertensives for rapid
control.23 Our patient’s BP was effectively treated at
the first seizure admission with clonidine and his PTA medications
(losartan, carvedilol, and minoxidil). On the second seizure admission
he required a nitroglycerin drip which is commonly used in hypertensive
emergency and was effective at controlling his BP.23We suspect the underlying cause of our patient’s hypertensive episodes
to be the frequently resistant nature of hypertension in patients with
ESRD in combination with anti-GBM disease. Although he was given
anti-epileptic medications as well, the patient did not have any
additional seizures after his BP was controlled. In addition, with BP
medication compliance as an outpatient, there have been no further
reports of additional seizures since his last admission.