neurological and non neurological causes of seizures in ICU set up. management of seizure disorder in ICU. EEG role in ICU set up. Status epileticus

1. Dr. Nisheeth M. Patel
M. D (Medicine), FCCCM
Consultant Physician & Intensivist

2.  Seizures complicate the course of about 3% of adult
patients admitted to intensive care units (ICUs) for
non-neurologic conditions and occur more frequently
in specialized neuroscience ICUs.
 Seizures are often the first indication of a central
nervous system (CNS) complication in these patients,
making their rapid etiologic diagnosis mandatory.
 Seizures can occur as a partial seizure or Generalized
tonic clonic seizure.
 Seizures occuring in ICU can either neurological or
non neurological; either new onset or in known case of
seizure disorder.

3. Classification of seizures: (ILAE)
 I. Partial seizures (seizures
beginning locally)
 A. Simple partial seizures (SPS)
 1. With motor symptoms
 2. With somato sensory or
special sensory symptoms
 3. With autonomic symptoms
 4. With psychic symptoms
 B. Complex partial seizures (with
impairment of consciousness) (CPS)
 1. Beginning as SPS and progressing
to impairment of consciousness
 A. Without automatisms
 B. With automatisms
 2. With impairment of
consciousness at onset
 A. With no other
features
 B. With features of SPS
 C. With automatisms
 C. Partial seizures
(simple or complex),
secondarily generalized

4. Classification Cont….
 II. Primary
generalized seizures
(bilaterally symmetric,
without localized
onset)
 A. Absence seizures
 1. True absence (“petit
mal”)
 2. Atypical absence
 B. Myoclonic seizures
 C. Clonic seizures
 D. Tonic seizures
 E. Tonic-clonic seizures
(“grand mal”)
(generalized tonic-clonic
[GTC])
 F. Atonic seizures
 III. Unclassified
seizures

5.  When seizures occur in ICU patients, clinical
judgment is required to apply this system, because
patients whose consciousness is already altered by
drugs, hypotension, sepsis, or intracranial disease may
be difficult to diagnose regarding the “simple” or
“complex” nature of their partial seizures.
 Status Epilepticus (SE) defines as more than 30 mins
of duration of either single episode of seizure ot
intermittent seizure without regaining consciousness
in between.
 SE can be divided into Generalized SE (Generalized
convulsive or non convulsive) or partial SE or Neonatal
SE.

6. Causes:
 Low anti epileptic Drug
level
 Stroke
 Metabolic disturbances:
 Hypo- Na+, Ca2+, Mg2+,
phospatemia
 Hyper & Hypo Glycemia
 Organ failure: Renal, Liver
 CNS infections:
Meningitis, Encephalitis,
TBM
 Cerebral anoxia/hypoxia
 Alcohol:
 Withdrawal
 Intoxication
 Head trauma
 Drug toxicity
 CNS tumour
 Immunological Disease
 Mitochondrial Disease

7. Changes in GCSE
 Hypoxia
 Respiratory acidosis
 Lactic acidosis
 Hyperpyrexia
 Hypertension (early)/hypotension (late)
 Hyperglycaemia (early)/hypoglycaemia (late)
 Tachycardia
 Cardiac arrhythmias

8. Seizure Recognition
 Three problems occur in ICU seizure recognition:
 Complex partial seizures in patients with already
impaired awareness
 Seizures in patients receiving neuromuscular junction
blockade
 Misinterpretation of movement disorders and
psychiatric disturbances as seizures.

9.  ICU patients often have altered awareness in the
absence of seizures, reflecting their underlying
condition, complications of those conditions (such as
septic encephalopathy), and drugs that depress
alertness.
 In this situation, an EEG is required to make the
diagnosis of a complex partial seizure
 Patients receiving neuromuscular junction blocking
agents will not manifest any of the usual signs of
seizures. Because most such patients receive
concomitant sedation with GABA agonists (e.g.,
benzodiazepines), the likelihood of seizures is small.

10.  The autonomic signs of seizures (hypertension,
tachycardia, pupillary dilation) are not readily
distinguished from the effects of pain or the patient’s
response to inadequate sedation.
 Any patient who manifests these findings and who has
a potential reason for seizures (e.g., intracranial
disease) should have an EEG to exclude this possibility

11. Manifestation of SE
 Primary GCSE usually begins as tonic extension of the
trunk and extremities, without any preceding focal
ictal activity.
 Less commonly encountered forms of GCSE
are myoclonic SE, in which bursts of brief myoclonic
jerks increase in intensity until a convulsion occurs.
 Myoclonic SE is particularly common in patients with
anoxic encephalopathy or metabolic disturbances,
particularly renal failure
 Clonic-tonic-clonic SE, in which a period of clonic
activity precedes the first tonic contraction.

12.  Secondarily Generalized SE in the ICU begins with a
partial (focal) seizure, which progresses to a tonic-
clonic convulsion.
 Very strong evidence of a structural brain lesion, care
should be taken to elicit evidence of any lateralized
movement.
 There are several forms of non convulsive SE (NCSE)
 Its very much imp for intensivist to diagnose NCSE as
it has detremental effect on cortical functions.
 NCSE may occur as a sequel of inadequately treated
GCSE

13.  As a rule, patients are expected to begin to awaken
within 15 to 20 minutes after the successful
termination of SE; Those who have not begun to
awaken after 20 minutes should be assumed to have
entered NCSE.
 This form of SE is sometimes termed subtle SE, and
careful observation will often reveal low-amplitude
clonic activity in some part of the body most
commonly, the face or the hands
 This condition requires emergent treatment under
EEG monitoring to prevent further cortical damage.
There are no clinical criteria, which indicate when
therapy has finally become effective

14.  EPC (Epilepsia partialis continua) is a special type of
partial SE in which repetitive movements are confined
to a small portion of the body (typically the thumb),
and may last for months or years. This type of SE is
most commonly associated with nonketotic
hyperosmolar hyperglycemia and does not respond to
conventional anticonvulsant treatment.

15. Diagnostic Approach
 New onset seizure:
 Observe the pattern of seizure
 Spot blood Sugar
 Urgent ABGA, electrolyte (sodium, potassium,
calcium, magnesium), urea
 Medication causing epilepsy
 Alcohol intoxication or withdrawal
 Brain imaging
 Check drug compliance, Blood AED level (both in case
if pt already on anti epileptic)

16.  Further investigations after stabilization
 Liver function tests, lactate, creatine kinase
 Toxicology screen
 Lumbar puncture
 Electroencephalogram
 Brain imaging with computed tomography or
magnetic resonance imaging

17. Management
 Assess A, B, C, GCS
 Give O2 and consider need for intubation/ventilation
 Monitor blood pressure, ECG, pulse oximetry
 Obtain i.v. access and draw blood for investigations
 Deciding whether to administer anticonvulsants to an
ICU patient who experiences a single seizure or a few
seizures requires a provisional etiologic diagnosis, an
estimate of the likelihood of seizure recurrence, and
an understanding of the utility and limitations of
available anticonvulsants.

18.  Patient who seizes during ethanol withdrawal will probably
not benefit from chronic anticonvulsant treatment
 Such a patient may need prophylaxis against delirium
tremens with benzodiazepines, but the seizures themselves
seldom require treatment.
 The patient who seizes during barbiturate or
benzodiazepine withdrawal, in contrast, should usually
receive short-term treatment (usually with lorazepam
[LRZ]) to prevent the development of SE.
 Seizures due to drug intoxications or metabolic
disturbances should similarly be treated for a brief period,
but do not indicate chronic anticonvulsant therapy.

19.  The ICU patient with CNS disease who has even a
single seizure should usually be started on a chronic
anticonvulsant regimen, with the decision to continue
medication reviewed prior to hospital discharge.
 Initiating anticonvulsant therapy after the
first unprovoked (e.g., not drug- or withdrawal-related)
seizure helps delay the onset of subsequent seizures,
but does not change their eventual incidence.
 Starting treatment after the first seizure in a critically
ill patient who has a condition predictive of seizure
recurrence may be even more important if the
patient’s problems include coagulopathies, myocardial
ischemia, or other conditions that would be seriously
complicated by a convulsion.

20. Brief Management of SE
 Assess A, B, C, GCS
 Give O2 and consider need for intubation/ventilation
 Monitor blood pressure, ECG, pulse oximetry
 Obtain i.v. access and draw blood for investigations
 If patient is hypoglycaemic, or if blood glucose
estimation is not available, give glucose:
 adults: give thiamine 100 mg i.v. and 50 mL of 50%
glucose i.v.
 children: give 2 mL/kg of 25% glucose i.v.

21.  Seizure control:
 A. Give benzodiazepine:
 diazepam: 0.2 mg/kg i.v. at 5 mg/min up to total dose of
20 mg;
 lorazepam: 0.1 mg/kg i.v. at 2 mg/min up to total dose of
10 mg;
 clonazepam: 0.01–0.02 mg/kg i.v. at 0.5 mg/min up to total
dose of 4 mg.
 If diazepam stops the seizures, phenytoin should be given
next to prevent recurrence.
 Repeat dose every 2–5 min if required. Note: risk of
respiratory depression with cumulative doses.

22.  If seizures persist, give phenytoin:
 phenytoin: 15–20 mg/kg (adults ≤50 mg/min; children
≤1 mg/kg/min) or fosphenytoin 15–20 phenytoin
equivalents (PE) mg/kg i.v. (adults ≤150 mg/min;
children ≤3 mg/kg per min).
 Additional doses of 5 mg/kg i.v., to a maximum dose of
30 mg/kg can be given for persistent seizures.
 Monitor blood pressure and the ECG during infusion.
If hypotension or arrhythmias develop, stop or slow
the rate of the infusion.

23.  If seizures persist (Refractory SE), intubate and ventilate
patient. Give either:
 thiopental: slow bolus 3–5 mg/kg i.v., followed by infusion
1–5 mg/kg per h, or
 propofol: slow bolus 1–2 mg/kg i.v., followed by infusion 2–
5 mg/kg per h,† or
 midazolam: slow bolus 0.1–0.2 mg/kg, followed by infusion
0.1–1.0 mg/kg per h.
 Titrate doses based on clinical and electrographic evidence
of seizures, targeting electrographic suppression of
seizures or EEG background suppression (isoelectric).
 Monitor BP and maintain normotension by reducing
infusion rate and/or giving fluids/pressor agents

24.  Insert nasogastric tube and administer usual
anticonvulsant medications if patient is receiving
treatment for pre-existing epilepsy.
 Beware of ongoing unrecognised seizures.
 Use EEG monitoring until seizures are controlled and
then for 1–2 hours after seizures stop. Continue to
monitor the EEG continuously, or for periods of more
than 30 minutes every 2 hours, during the
maintenance phase.
 Avoid muscle relaxants (use continuous EEG if giving
repeated doses of muscle relaxants)

25.  Discontinue midazolam or thiopental, or start
reducing propofol, approximately 12 hours after
resolution of seizures.
 Use continuous EEG monitoring and observe for
further clinical and/or electrographic seizure activity.
 If seizures recur, reinstate the infusion and repeat this
step at 12–24-hour intervals or longer if the patient’s
seizures remain refractory.
 Look for and treat cause and precipitant.
 Look for and treat complications: hypotension,
hyperthermia, and rhabdomyolysis.

26. Controversial Management Issues
 Periodic lateralized epileptiform discharges (PLEDs).
 PLEDs are an EEG phenomenon usually seen in the setting of
large acute strokes or rapidly expanding mass lesions (e.g.,
tumors or abscesses). Less commonly, acute metabolic or toxic
disorders will “reactivate” PLEDs in the vicinity of an old lesion.
 The EEG activity signifies the repetitive, synchronous firing of
large numbers of neurons near the lesion; there is occasionally
contralateral myoclonic jerking of the hand or face.
 Patients who have clinical seizures (i.e., other than the
myoclonic jerks) should receive anticonvulsants.
 The myoclonic movements associated with PLEDs are difficult to
suppress without resorting to high-dose barbiturates or
benzodiazepines.
 The data available do not suggest that suppressing the electrical
phenomenon improves outcome.

27. Epilepsia partialis continua
 EPC: Isolated repetitive movement (usually of the
hand or face), often following an infectious or vascular
insult, or in the setting of nonketotic hyperglycemia.
 The movement may persist for months or years.
 Most patients receive anticonvulsants to prevent
spread of the discharge, but these agents seldom affect
EPC itself.
 Attempts at treatment with high-dose barbiturates
result in short-term suppression of the movement, but
it usually returns as the drug levels decline.

28. Prognosis:
 Three major factors determine the outcome of SE: the type
of SE, its cause, and its duration
 GCSE carries the worst prognosis for neurologic recovery as
a consequence of SE itself;
 Myoclonic SE following an anoxic episode carries a very
poor prognosis for survival.
 CPSE produces some risk of limbic system damage, usually
manifested by memory dysfunction.
 Simple partial SE may produce neuronal damage, but this
is difficult to discern from the effect of the lesion that
commonly produces this form of SE.
 Absence SE does not seem to carry a risk of neurologic
deterioration

29. THANK
YOU