UHM 2018, Vol. 45, No.

1 – HBO2 for late sequElae in co poisoning: CASE

Case Report
Hyperbaric oxygen for late sequelae of carbon monoxide poisoning
enhances neurological recovery: case report
Lon W Keim, MD 1; Sreekanth Koneru, MD 2; Vesper Fe Marie Ramos, MD 2; Najib Murr, MD 2,
Deborah S. Hoffnung, PhD 3; Daniel L. Murman, MD 2; Jeffrey S. Cooper, MD 1;
Diego Torres-Russotto, MD 2
Hyperbaric Medicine Center, Nebraska Medicine, Omaha, Nebraska U.S.
1

2 Department
of Neurological Sciences, University of Nebraska Medical Center,
Nebraska Medical Center, Omaha, Nebraska U.S.
3 Department of Neuropsychology, CHI Health, Omaha, Nebraska U.S.

CORRESPONDING AUTHOR: Jeffrey S. Cooper – jeffrey.cooper@unmc.edu

_____________________________________________________________________________________________________________________________________________________________________

ABSTRACT
Neuropsychiatric sequelae have been reported in 15%-45%
of survivors of carbon monoxide (CO) poisoning. Hyperbaric
oxygen (HBO2) therapy reduces the incidence of cognitive and
neurological a dysfunction. The efficacy of providing HBO2 be-
yond the first one to two days after initial insult is unknown.
However, some evidence exists for the benefit of this treat-
ment. We report on treating a patient 14 months after CO injury,
who responded with markedly improved neurologic status.
A 27-year-old scholar was found comatose due to CO poison-
ing (carboxyhemoglobin = 31.7%). He received five acute
HBO2 treatments. After discharge, he developed chorea, Parkin-
sonism, dystonia, memory loss, slowed processing speed and
verbal fluency, leaving him disabled. After the patient reached a
clinical plateau, HBO2 was tried again at 90 minutes at 2.4 ATA
plus air breaks. Neuropsychological testing was performed at
baseline and after each 20 HBO2 cycles, five of which were per-
formed during the period from 14-22 months after CO exposure.
After the first 20 treatments, Parkinsonism and dystonia
improved. After 40 sessions, further improvements were seen
on mental speed, verbal fluency, and fine motor movements.
The outcome following 100 treatments was that the patient
regained independence, including the ability to drive and
to become gainfully employed.
Our case calls into question the concept that HBO2 therapy
has no role during the chronic phase of CO brain injury.
Randomized clinical trials should be considered to evaluate the
therapeutic efficacy of HBO2 in patients with neurological se-
quelae following CO injury.
Introduction
Carbon monoxide is one of the most common causes
of poisoning in the United States [1] and may be re-
sponsible for one-half of all fatal poisonings worldwide
[2,3]. Delayed or persistent neuropsychiatric sequelae,
including apathy, gait disturbances, movement disorders,
seizures, hallucinations, and dementia, have been re-
ported in 15%-45% of survivors after apparent recovery
[4,5]. One hundred percent oxygen, administered im-
mediately following initial rescue, is the standard of
care. Hyperbaric oxygen (HBO2) therapy within the
first 24 hours of care is believed to offer additional
benefits, and is recommended for those patients with
or those who are at risk for neurologic sequelae [6].
HBO2 reduces the incidence of cognitive and neuro-
logical dysfunction by 46% at six weeks and 12 months
from exposure [7]. The therapeutic efficacy of provid-
ing HBO2 beyond the first one to two days after initial
insult is unknown and generally unaccepted. Howev-
er, some evidence exists for its potential benefit [8,9].
We report using HBO2 to treat a patient 14 months
after carbon monoxide injury, with resulting mark-
edly improved neurologic status. This is one of only
a few reports of beneficial HBO2 initiated longer than
a year following initial exposure. Further studies evalu-
ating the potential benefit of HBO2 after the acute
phase of carbon monoxide poisoning are warranted.

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KEYWORDS: carbon monoxide poisoning; hyperbaric oxygen; delay to treatment

Copyright © 2018 Undersea & Hyperbaric Medical Society, Inc. 83

 UHM 2018, Vol. 45, No. 1 – HBO2 for late sequElae in co poisoning: CASE
Case report
A 27-year-old, previously high-functioning scholar-
athlete was found in a garage, with two cars running,
following a suicide attempt. He was brought to our
institution’s emergency department (ED), where we
estimated his time of exposure to be two to two and
a half hours. He was unresponsive when found and was
intubated at the scene. His Glasgow Coma Scale (GCS)
was 3, with rigid extremities, and he had sustained
bilateral clonus. He began to experience seizures shortly
after arrival at the ED.
Initial laboratory testing revealed arterial pH 7.22,
HCO3 16, lactate 7.1, carboxyhemoglobin 31.7%,
troponin 0.06, and an echocardiogram suggesting global
hypokinesia. Magnetic resonance imaging (MRI),
performed two days after exposure, revealed diffusion
restriction and increased signal on T2-weighted (T2W)
and attenuated inversion recovery (FLAIR) in the bilat-
eral globus pallida, hippocampi and parahippocampal
gyri (see Figure 1).
The patient received five initial HBO2 treatments.
Although afebrile on admission, within three hours of
admission he developed what was considered to be
a rather profound central fever, with temperatures
reaching 39.6°C. Fever compromised his HBO2 therapy
for fear of high oxygen tension-induced seizures. He
required ventilator support initially, but was extubated
on Day 2 and remained in the hospital for 14 days. He
received one 90-minute HBO2 treatment at 3.0 atmos-
pheres absolute (ATA) on Day 1 (14 hours post-
arrival), a 45-minute HBO2 treatment at 3.0 ATA on
Day 2, a 30-minute HBO2 treatment at 3.0 ATA on
Day 5, and a 90-minute HBO2 treatment at 2.4 ATA
for 90 minutes each daily on Days 6, 7 and 8. All treat-
ments were in Sechrist monoplace chambers. After
extubation, air breaks were provided by non-rebreather
facemask on treatments. The short treatments and lack
of treatments on Days 3 and 4 were due to agitation
following extubation.
The patient was discharged to an outpatient rehabil-
itation program due to cognitive deficits in learn-
ing, memory, visual, attention, verbal fluency, mental
speed, complex attention, and motor coordination. He
stayed with his family for supervision and assistance.
Within two months he developed chorea and dystonia.
By 90 days after poisoning, he had developed Parkin-
sonism and severe dystonic symptoms in the neck, with
84
FIGURE 1: Magnetic resonance imaging, performed
two days after exposure, revealed diffusion restriction
and increased signal on T2-weighted (T2W) and
attenuated inversion recovery in the bilateral globus pallida,
hippocampi and parahippocampal gyri.
overflow blepharospasm. Dystonia and tremor were
present bilaterally in the upper extremities, and lower
-extremity dystonia was resulting in falls. Additional
symptoms included short-term memory loss and se-
verely slowed processing speed affecting visuospatial
functioning. Naming and verbal fluency were affected
as well. The dystonic symptoms were the most dis-
abling, preventing cooking, self-feeding, ambulation
and dressing. Amantadine, levetiracetam, baclofen and
botulinum toxin injections were administered, with
little benefit.
At six months, the patient’s symptoms appeared to
have reached a clinical plateau, and his family consult-
ed our team. We explained to the family that the tra-
ditionally accepted therapeutic window for HBO2 had
likely passed. Over the next several months, however,
with no further improvement and in consultation with
neurology, a suggestion was made to try HBO2 therapy
again because of the persistent and disabling nature
of his symptoms. This was agreed upon by the patient
and his family members.
The medical team agreed that a reasonable treatment
trial would be to treat the patient in blocks of 20 sessions,
and to stop at any point he had recovered to normal
Keim LW, Koneru S, Ramos VFM, et al.
 UHM 2018, Vol. 45, No. 1 – HBO2 for late sequElae in co poisoning: CASE

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Table 1: Timeline of evaluations

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HBO2 treatment numbers 0 0- 21- no 41- 31- 81- follow-up

20 40 HBO2 60 80 100 evaluation
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evaluated after treatment number: 21 40 70 97

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months from injury 14 16 17 18/19 20 21/22 23 70

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months from starting treatment 0 1 2 3-4 5 6-7 8 55

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MOCA (26-30 is “normal”) 23 22 23 29 30 28

movement __________________________________________________________________________________________________________________________

disorders UPDRS - Part III (motor)(0-132) [1] 40 10 8 10 8

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clinic
Fahn-Marsden Dystonia scale (0-120) 41 34 4 4
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neuropsychology verbal fluency -5 +6 +9

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word memory -11 -11 -7

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mental speed (written) +1 +5 +10
__________________________________________________________________________________________________________________________

mental speed (oral) -3 -1 +4

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mental and motor speed +3 0 +4

__________________________________________________________________________________________________________________________

fine motor speed (right) +4 +6 +12

__________________________________________________________________________________________________________________________

fine motor speed (left) -1 0 +6

_________________________________________________________________________________________________________________________________________________

functional levels. Further, it was agreed to continue
treating him for as long as he improved and as long
as he and family members agreed to the treatment.
This protocol used neuropsychiatric evaluation every
20 treatments to give us an objective treatment end-
point (clinical plateau or resolution of symptoms).
Since this treatment was not considered research but
rather innovative therapy, a reduced facility fee was
assessed, and professional fees were waived.
Neuropsychological examination and testing with
video documentation was performed by neuropsycho-
logists and movement disorders specialists at baseline
and after approximately each 20 HBO2 cycles – similar
to a prior study by Myers, et al. [10]. All treatments
were provided via Sechrist monoplace chambers (two
hours each for 90 minutes at maximum pressure of
2.4 ATA), with time provided for compression and
decompression (10-15 minutes each), and five-minute
air breaks provided by non-rebreather facemask twice
(i.e., every 30 minutes) during the period of maximum
pressure. Five cycles of 20 daily treatments each were
performed during the period from 14-22 months after
CO exposure. The patient’s improvement was assessed
as having plateaued during his fifth cycle of treatment
(100 exposures in total), with no significant changes seen
between assessments after the 70th and 97th treat-
ments.
After the first 20 treatment sessions, Parkinsonism
and dystonia markedly improved. The Unified Parkinson
Disease Rating Scale Part III (UPDRS scale is 0-132, with
0 being normal [11]) decreased from 40 to 10, and the
Fahn-Marsden Dystonia scale from 41 to 34 (0-120, 0
being normal). The patient’s tremor disappeared. With
further treatments, he was able to write and grip with
his hands, leading to significant increase in life func-
tion abilities. His plantar inversion improved, leading to
better ambulation with no falls, and formal measures
on neuropsychological testing (see Table 1) improved.
His Montreal Cognitive Assessment (MOCA) improved
from 22-23 at baseline to 28-30 (total possible score is
30 points; a score of 26 or above is considered normal).
Although some cognitive areas had no clear change,
after 40 sessions the greatest improvements were seen
on mental speed (written and oral), verbal fluency and
fine motor movements (Table 1). Eventually, 100 treat-
ments were completed, with the most relevant outcome
that the patient regained independence, the ability
to drive, and to be gainfully employed (Figure 2).

Keim LW, Koneru S, Ramos VFM, et al. 85

 UHM 2018, Vol. 45, No. 1 – HBO2 for late sequElae in co poisoning: CASE

Discussion
In a rat model of stroke, delayed HBO2 therapy has
shown induction of cell proliferation in damaged brain
areas [12]. HBO2 treatment during the subacute phase
(16 hours to 12 days) of CO poisoning has been re-
ported to be beneficial in a few cases [8,9,5]. How-
ever, benefit has been reported even after initiating
HBO2 therapy seven months post-injury [1]. Indeed,
one case of CO-induced visual impairment was treated
four years after exposure to good effect [13]. Myers re-
ported five patients impaired by chronic CO exposure,
two of whom were exposed for 16 months or more
due to faulty appliances [10]. All five had marked
improvements after 10-59 HBO2 treatments.
Additionally, support exists for the use of HBO2 in a
variety of brain injury conditions including moderate
to severe traumatic brain injury [14,15], stroke [16],
cerebral palsy [17], and other chronic neurological
disorders [18].
Our case is unusual, if not unique, given that the
period from acute HBO2 treatment to delayed HBO2 FIGURE 2: The patient regained independence, the
treatment is one of the longest reported, occurring ability to drive and to be gainfully employed.
more than one year after initial injury. Our patient Here he celebrates his recovery with ziplining in Mexico.
also experienced almost complete resolution of neuro-
logical deficits, and although we anticipated some im-
provements, this was most unexpected. Several factors
might be considered for the degree of benefit, including We can only speculate about possible mechanisms
patient age, general health, and function before injury. of recovery. New neurons could be generated, or so-
Up to 75% of patients with CO-induced neurologic called “idling” or “hibernating neurons” could be re-
sequelae are reported to resolve without treatment by activated. Improved angiogenesis or enhanced mito-
one year post-insult [19,20]. However, the 25% who chondrial function could also have a role, as could stem
remain impaired generally do not spontaneously im- cell mobilization. It is possible for viable but otherwise
prove. Weaver reported four cases of CO-induced marginally functioning neurons to be revitalized, thus
coma that had good resolution by six months without facilitating regeneration of prior axonal tracts.
HBO2 intervention, but these cases demonstrate spon- Nevertheless, our case calls into question the assump-
taneous resolution in a rather steady fashion from the tion that HBO2 therapy has no treatment role during
point of insult on [21]. Deterioration over a period of the chronic phase of CO-induced brain injury. Clinical
months that was followed by nearly a year of unchanging trials should be considered to evaluate the therapeutic
deficits despite ongoing physical and occupational efficacy of HBO2 in patients with neurological sequelae
therapy suggests injury that is likely permanent and following CO injury. These could be done similarly as
thus unlikely to further resolve spontaneously. Although in our case, in block fashion, with one- to two-month
physical and occupational therapy continued during breaks from treatment, to serve as self-control (as-
the period of HBO2, a marked improvement was seen sessments done before and after each block) similar
only with the addition of HBO2. to crossover studies. Registry studies could also serve
The mechanisms for our patient’s recovery are un- to recruit a significant number of subjects prior to
known. Adult brains have been found to have stem or investing in randomized controlled studies. In any event,
progenitor cells that can help in neural regeneration the establishment of controlled studies is suggested
[22]. These processes tend to be oxygen-dependent [23]. here as both highly relevant and important.

86 Keim LW, Koneru S, Ramos VFM, et al.

 UHM 2018, Vol. 45, No. 1 – HBO2 for late sequElae in co poisoning: CASE
We acknowledge that this patient was treated out-
side existing UHMS guidelines for CO poisoning. As
such, he was assessed a reduced facility charge and no
professional fees. While we cannot endorse the admin-
istration of similar treatment based upon one patient’s
experience, we feel that the case brings into question
the presumption that HBO2 has no role in the treat-
ment of chronic brain injury from CO poisoning.
Clinical trials should be considered to evaluate the
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