Reminder of important clinical lesson

CASE REPORT

Temporary recovery after resuscitation: delayed
postanoxic encephalopathy
Stephan Goedee,1 Gerarda A M van der Nat,2 Gerwin Roks1
1

Department of Neurology,
St Elisabeth Hospital, Tilburg,
The Netherlands
2
Department of ICU,
St Elisabeth Hospital, Tilburg,
The Netherlands
Correspondence to
Stephan Goedee,
stephangoedee@gmail.com

SUMMARY
Delayed postanoxic encephalopathy is reported
infrequently and is characterised by a lucid interval of
seemingly good recovery from an anoxic insult. Days or
even weeks may pass before changes in behaviour,
motor responses or consciousness occur. Neurological
deterioration may progress to coma, death or severe
disability, whereas some patients have a second recovery
period. Pathogenesis is yet to be discovered. Prognosis is
reportedly poor, treatment is symptomatic and at best
anecdotal. We present a case report and available
literature.

BACKGROUND
It is important to recognise the delayed onset of postanoxic encephalopathy in the clinical setting of a
lucid interval of seemingly good recovery from an
anoxic insult. It has been reported throughout
medical literature in a small number of case reports
and carries a poor prognosis. Classically, there is a
lucid interval after initial good recovery from an
anoxic insult, upon which neurological deterioration
may progress to coma, death or severe disability.

CASE PRESENTATION
A 69-year-old man was seen at the emergency
department after he had been resuscitated by a
neighbour. She had found him unconscious and
pulseless, upon which she had initiated resuscitation. Upon arrival of the paramedics he had spontaneous circulation and was agitated. Because of
vomiting and aspiration he was intubated for
airway protection. His medical history reported
hypertension and diabetes mellitus type 2.
At presentation at the hospital his Glasgow
Coma Score was 3, with anisocoria and absent oculocephalic reflex but intact pupillary light and
corneal reflexes. His circulation was stable with a
blood pressure of 200/100 mm Hg and a regular
pulse. Oxygenation was insufficient and required
mechanical ventilation using 100% oxygen. After
24 h the patient gradually improved.

INVESTIGATIONS

To cite: Goedee S, van der
Nat GAM, Roks G. BMJ
Case Rep Published online:
[please include Day Month
Year] doi:10.1136/bcr-2013008918

Laboratory examination showed a lactic acidosis
(lactic acid 5).
CT scan of the brain revealed no abnormalities,
nor did an additional CT angiography.
ECG revealed ST-depression mostly over the anterior cardiac wall. This was confirmed by echocardiography, which showed no movement of part of the
anterior wall. Furthermore, the ECG revealed a suspicion of Wolff-Parkinson-White (WPW) syndrome.

Goedee S, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-008918

The troponin T levels were elevated with a
maximum of 0.2 mg/l (normal value 0.0–0.1 mg/l).
We concluded an arrhythmia caused by anterior
myocardial infarction or possibly a previously
unknown WPW syndrome as a cause of the cardiac
arrest.

OUTCOME AND FOLLOW-UP
At the intensive care unit he recovered to a
maximum neurological score of opening his eyes on
verbal command and flexing his legs on demand.
However, movement in his arms appeared to be
limited to only flexing on pain. There was no clear
visual orientation and he still depended on mechanical ventilation. After 4 days, he deteriorated after a
generalised tonic–clonic seizure. Prior to this he had
not revealed any seizure-like activity. Therefore this
was considered symptomatic upon which Valproate
was initiated. EEG revealed no epileptic activity.
Subsequent serial EEG recordings showed sharpwave complexes at the vertex (figure 1), which
ceased on a bolus of Midazolam. Hence treatment
was intensified with intravenous Phenytoin,
however without improvement. An MRI scan of the
brain showed hyperintense zones on T2-weighted
images compatible with cortical laminar necrosis
(figure 2). After nearly 3 weeks he showed no
further improvement other than opening his eyes on
verbal command without goal-directed eye movements and pathological flexing of the arms on pain
without movement of the legs. A second MRI of the
brain displayed an increase in the previously found
hyperintensities (figure 2). Despite maximal treatment the clinical situation remained poor and treatment was stopped.

DISCUSSION
The patient we presented deteriorated after initial
clinical improvement from postanoxic coma. After
ruling out several causes such as non-convulsive
status epilepticus, basilar artery thrombosis and
metabolic causes, a delayed postanoxic encephalopathy was diagnosed. As early as in 1917, a woman
was described with initial full recovery after strangulation followed by a severe neurological deterioration after 5 days.1 Autopsy revealed grossly visible
cavities in striatum and caudate nucleus, but an
otherwise intact brain. Several other case reports
followed up to a comprehensive overview of five
cases in 1962.2 The lack of awareness of delayed
postanoxic encephalopathy was already noted in
this paper and is still reflected by the scarce subsequent reports.
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Reminder of important clinical lesson

Figure 1 EEG on day of deterioration, 5 days after initial good recovery from anoxic insult, revealing sharp-wave complexes at the vertex.
Little is known about the true incidence of delayed postanoxic encephalopathy, ranging from a reported 1–28/1000 in
patients experiencing a hypoxic event.2–5 A variety of symptoms
may mark the unexpected neurological deterioration, which
develops within 1–4 weeks; parkinsonism, tetraparesis, pseudobulbar palsy, sphincteric incontinence, apathy or agitation even
up to manic behaviour.1–6
The brain is susceptible to a variety of hypoxic causes;
reduced global blood level of oxygen (drowning, airway obstruction, reduced inspired oxygen content), circulatory failure,
carbon monoxide intoxication, hypoglycaemia (blocking oxidative metabolism and thereby halting intracellular respiration).7
How these events lead to delayed postanoxic encephalopathy,
which is so typically marked by a lucid interval of ‘pseudorecovery’, remains to be discovered. Several pathophysiological
mechanisms have been proposed throughout literature, none
however conclusive. The reported findings at autopsy note
extensive demyelination sparing the subcortical arcuate fibres,
degeneration of striatum and caudate nucleus, no significant
blood vessel abnormalities and accumulation of fat-laden macrophages.2–5 Neuroimaging also shows these typical lesions at
basal ganglia and cortical laminar necrosis. CT may reveal a
hypodense striatal region, whereas MRI is more sensitive and
shows hyperintense signals in the basal ganglia or in the white
matter in the arterial watershed zones and along the gyri, especially on fluid-attenuated inversion recovery and diffusionweighted images.5 7–12 More advanced techniques such as

positron emission tomography-MRI and susceptibility-weighted
MRI (SWI) look promising, but they are not available in most
clinical settings.13 14
In the presented case the CT scan appeared normal, however
subsequent MRI scans of the brain showed progressive cortical
laminar necrosis.
Prognosis of delayed postanoxic encephalopathy is reportedly
poor. The neurologic deterioration may progress to coma, death
or severe disability, although some patients may have a second
recovery period.2–5 Treatment is predominantly symptomatic.

Learning points
▸ Every patient who presents with changes in behaviour,
motor responses or consciousness upon a lucid interval of
seemingly good recovery from an anoxic insult, should be
considered as possibly having a delayed postanoxic
encephalopathy.
▸ Classically there is a lucid interval after initial good recovery
from an anoxic insult, upon which neurological deterioration
may progress to coma, death or severe disability.
▸ Other causes such as a non-convulsive status epilepticus
must be ruled out and treated when diagnosed.

Figure 2 Fluid-attenuated inversion
recovery-weighted MRI, revealing
cortical laminar necrosis and
periventricular white matter lesions, at
4 days after an anoxic insult (A) and
18 days on deterioration (B and C).

2

Goedee S, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-008918

Reminder of important clinical lesson
Competing interests None.

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Provenance and peer review Not commissioned; externally peer reviewed.
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5
6
7

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Goedee S, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-008918

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