5 years of Critical Care EEGs

5 years of Critical Care EEGs – 5 Lessons Learnt
Dr Andrew Bailey (ST 6+ Anaethetics)
Dr Larry Mulleague (Consultant Intensivistand Anesthetist)
Epsom and St. Helier University NHS Trust
Introduction
Electroencephalography (EEG) is used in neuro-diagnostics of thecritically ill
patient1 to
- characterise paroxysmal clinical events (behavior, sensory perception, or
motor activity) that might be seizures (abnormal neuronal activity).
- detect non-convulsive or clinically subtle seizures
- distinguish coma from diminished responsiveness due to other causes
(psychiatric, sedation, neuromuscular, cortical de-efferentation/locked in
syndrome)
ILAE classification of seizures determines them to be eithergeneralised (bilateral),
focal (unilateral) and focal with bilateral evolution. Epilepsy is defined as at least
two unprovoked (or reflex) stereotyped attacks occurring more than 24 hours
apart2.The assessment of neurologic dysfunction clinically is very difficult in the
critically ill due to the presence of many metabolic /pharmacological factors
altering consciousness (encephalopathic)&applying diuress to provoke seziures.
Critical Care EEG can be helpful with certain syndromes
- Metabolic
- Anoxic
- Infective
- Toxic
Aim
1)
2)
3)
4)
5)
Identify percentage contribution of the above syndromes referred for EEG.
Identify how EEG correlated or aided confirmation of the above syndromes.
Assess the impact of repeat EEGs
Identify risk factors for poor neurological outcome.
Identifies areas of referral improvement
Methods
This was a retrospective study of DGH patients who underwent EEG monitoring
over a 5-year period. Patientreferrals were classified into one of the following.

Metabolic encephalopathy

Anoxic encephalopathy

Neurological infection

Toxic encephalopathy

Endocrine disorder

Seizures (referral question does not elude to underlying pathology)

Hypertensive encephalopathy

Epilepsy

Repeat
The primary outcome measure was whether the report explicitly answered the
referral question.
Results
Data from 1/4/2008 till 22/08/2014 excluding 1/4/2011 till 08/08/2012 due to
missing data log. In total 60 months were studied yielding 71. Four however had
noavailable EEG record therefore 67 studies were analysed with an average age of
52 years.
Identify percentage contribution of the above syndromes referred for EEG.
Most of referrals for EEG appear to be relating to seizures and anoxic
encephalopathy, accounting for almost a third each. The next most common reason
was as a repeat EEG (17%) and then metabolic encephalopathy (10%) and
neurological infection (7%).
Referal question
Metabolic
encephalopathy
10%
Epilespy
2%
Repeat
18%
Toxic
encephalopathy
3%
Hypertensive
encephalopathy
2%
Anoxic
encephalopathy
28%
Seizures
30%
Neurological
infection
7%
Identify how EEG results correlated or aided confirmation of the above syndromes.
Anoxic encephalopathy; of nineteen cases only two reports explicitly confirmed
anoxic encephalopathy. Fiveindirectly supported its diagnosis by the observation
of triphasic and BIPED seizure activity and featureless EEGs. Four explicitly
reported inconclusive test with two noting encephalopathy, one attributed to
propofol. Five reports simplydescribed waveform activity with no application to
the clinical picture.
Nine of nineteen patients referred for EEG with the referral question of anoxic
encephalopathy died. Half died within five days of the EEG where as the remaining
patients took between 1-3 months. Six patients were referred for anoxic
encephalopathy studies that had no history of CPR but four of these six patients
had significant chest sepsis as primary critical care pathology.
Seizure group; we once again see a heterogenic group of reports.
- 4 inconclusive
- 3 propofol encephalopathy
- 4 encephalopathy
- 3 anoxic encephalopathy
- 4 waveform analysis with no reference to the clinical picture.
- 1 syptomatic epilepsy but not status
Repeat group, twelve cases in total.
- 1minimal improvement
- 1 repeated post propofol encephalopathy and noted grossly abnormal
- 1 repeated post inconclusive result to confirm anoxic encephalopathy.
- 9 were no change. Their initial reported syndromes being
o 2 neurological infections
o 4 anoxic encephalopathy
o 3 were on the same patient regarding seizures where the initial EEG
suggest anoxic encephalopthy
Propofol grouponly one patient was re-tested of the four.
Metabolic
encephalopathy
2%
Propofol
encephalopathy
9%
Reported Result
No Change
18%
Normal
2%
Encephalopathy
16%
Nil conclusive
29%
Anoxic
encephalopathy
13%
Featureless
11%
Conclusions
As would be expected most EEGs were to aid the diagnosis of anoxic
encephalopathy and seizures. The former requires clear communication between
the referring team and with whom the EEG is analysed. With almost a quarter of
these reports simply having waveform analyse this may prove a barrier to the
intensivist’s application of the result with the patients future care pathway. EEGs
have no role in the determination of brain death. It is a surface brain study and
therefore limited in its ability at describing brain stem activity. An iso -electric or
wholly unreactive EEG however may aid relatives in acknowledging futility1 .
Patientslabelled as seizure with no explicit neurological syndrome
documented,demonstrated no incidence of status. Understandably a third of these
patients’ reports were inconclusive or once again were solely waveform analysis.
One patient was referred to aid the diagnosis of epilepsy. Noting epilepsy’s
definition being two unprovoked seizures and the average critical care phenotype
often possessing several provoking factors, one must question the usefulness of
such a referral.
Abnormal movements often pose the intensivista diagnostic challenge. Grimacing,
chewing, or nystagmoid eye movements; abrupt and otherwise unexplained
changes in pulse, blood pressure or respiratory pattern; or abrupt deterioration in
conscious level may all be clinical events caused by abnormal neuronal activity
(seizures)1. The greatest fear is to miss non-convulsive status eplilptics (NCSE),
which should be anticipated in those with a prior history of epilepsy, any intracranial event or infection. Our study however shows that NSCE has an incidence of
less than 1in70 patients referred for EEG.
One otherfinding that may have an impact on future patient management concerns
those patients reported as propofol encephalopathy. Only one had a repeat study,
which questions the necessity of the initial referral. Those patients who did
undergo a repeated EEG on the whole had no change in report. No change should
still be seen as a positive result as it adds weight to the initial EEG findings.
Risk factors for poor neurological outcome, seem to be those patients who have
received CPR but also those with significant chest sepsis.
Areas of referral improvement identified were
a. Explicit questions in the referral.
b. Tick box for poor neurological outcome risk factors
c. Post-EEG one on one discussion between consultants (e.g.
gastroenterologist doing an urgent OGD or radiologist interrupting a
critical care CT)
References
1. SJM Smith, EEG in neurological conditions other than epilepsy: when does it help,
what does it add? J NeurolNeurosurg Psychiatry 2005;76:ii8-ii12
2. SJM Smith, EEG in the diagnosis, classification, and management of patients with
epilepsy. J NeurolNeurosurg Psychiatry 2005;76:ii2-ii7