Neck Injury Prognosis and Treatment
portert at skyfox.usask.ca
portert at skyfox.usask.ca
Mon Sep 11 05:43:46 EST 1995
I am posting this message seeking miscellaneous thoughts and as a follow up on
My daughter was born 10 months ago hypotonic and with paralyzed diaphragms.
The initial hypothesis of hypoxic ischemic encephelopathy was quickly ruled
out. The long standing hypothesis was a discrete stroke in the c4-c5 region,
mainly because the hypotonia had resolved itself to a great extent (a left
right asymmetry remains), and no other problems can be found.
Her presentation, today, is mechanical ventilation during night time sleep
and respiratory aids during the day. The two respiratory aids are an Easy-
Breather and a T-piece. The first is a sponge cap that sits on top of the
tracheal tube and delivers some oxygen. The T-piece is a tube with a
humidified flow of oxygen rich air passing over the tracheal tube. These
respiratory aids provide no mechanical support - she must breathe on her own.
She is capable of doing this because her diaphragms are no longer paralyzed.
Her left diaphragm was confirmed to be active at two months after birth. The
right diaphragm was confirmed to be working two months after that. In
addition, she has demonstrated a respiratory drive from birth. Before her
diaphragms could move, and when challenged (i.e., mechanical ventilator
support was removed), she would panic and make what were described as
breathing motions with her upper chest and neck.
The prevailing hypothesis of a discrete stroke in the c4-c5 region is not
consistent with this presentation. If there was a stroke causing nerve
damage, and presumably scar tissue, then how could her diaphragms have begun
to move two and four months after the stroke and continue to improve today?
Some of the physicians involved still speak of a lesion caused by a stroke
(two MRI's, CT scans, Evoked Potentials and other tests have not confirmed a
lesion), one physician and myself speak of a neck compression injury confirmed
only by her continuing improvement.
This is a debate that has important implications about prognosis and
treatment. Before I solicit opinions on the prognosis and treatment, I
welcome any opinions on the debate so far presented with its limited
The prognosis differs for the two hypotheses. If the injury was a stroke,
then there is a very specific maximum recovery that is possible. If the
injury was a neck compression injury, then the extent of the recovery depends
on her development and treatment. In particular (and here is the rub), if
the treatment is aiming at a specific limited recovery following a stroke but
the injury is a neck compression injury, then does the treatment become a
self-fulfilling prophecy? By assuming she must be ventilated at night and
weaning her onto a night-time (volume control) ventilator, does this inhibit
attempts to wean her off of all ventilators.
If the injury is a stroke, then she will have to be ventilated at night with
no chance of recovery according to some physicians. If the injury is nerve
compression/ rotation/ elongation, then the nerve damage may require two or
more years to resolve. Some resolutions can be complete, some cannot.
Examples of this are neck compression injuries suffered by football players.
Some of these people walk out of the hospital, and some do not.
Thus, I have presented a portion of the main debate: how to treat my daughter.
Speculations are welcome at this point also, but I am sure that more
information is needed by anyone in cyber-space who is still interested in my
In any event, my daughter's treatment is a weaning attempt. Some physicians
what to wean her off a Seimans 300 or 900c onto a Bear home ventilator or a
Puritan-Bennett home ventilator. Others want to wean her off of all
ventilators. The differing opinions, I believe, revolve around the unstable
nature of her sensitivity/insensitivity to high entidal CO2 levels.
Until a week ago, my daughter's respiratory support was:
- 6 to 11 hours a day supported by the T-piece (oxygen rich air flowing
over the tracheal tube) with entidal CO2 levels ranging from 60 to 75;
- 1 or 2 hours a day with the Easy Breather (sponge cap over the
tracheal tube, with a low flow of oxygen) with entidal CO2 levels
ranging from 65 to 80; and,
- the remaining time, mostly at night, on a Seiman's 300 or 900c
ventilator set to SIMV plus Pressure Support. The SIMV rate was 14
and the Pressure Support was 6 or 8 cm. (I do not recall the Pressure
Support settings). The entidal ranges are from 60 to 75.
Now she receives almost the same support from respiratory aids, but is on an
Assist/Control volume support from a Puritan-Bennett volume ventilator with
the IMV rate set at 30 breaths per minute. She is effectively prohibited from
initiating her own breaths at this rate. This is why I am concerned that
some of the physicians involved have resigned themselves to night time
ventilation for the rest of her life.
The entidal ranges while on volume Assist/Control, IMV of 30, are 50 to 60.
Her entidal levels while on the respiratory aids are slightly higher then
previously. The whole issue is complicated because she is teething, so I
cannot say these levels are truly higher.
The weaning protocol, as it is, is to reduce the IMV rate slowly, by two
breaths once or twice a day. I want it reduced quickly. I want this because
in the past when we reduced SIMV and Pressure Support levels, the trigger
level of entidal CO2 gradually rose. We have witnessed a variable chemical
sensitivity to entidal CO2 volumes.
At one point, the SIMV + Pressure support was down to 10 breaths per minute
and 6 or 5 cm of pressure. When the settings where this low, she would not
be triggered to breathe on the respiratory aids until the entidal CO2 values
rose to 80 or 90. The current IMV setting of 30 will not cause the entidal
CO2 levels to rise when she is off of the ventilator, but as this rate is
gradually reduced, then the trigger level for her breathing will gradually
rise. If this is true, then this weaning protocol may simply wean her onto
the volume control ventilator with a IMV rate above 15 or 20 at night for the
rest of her life, rather than off of ventilators in general.
I am not arguing that the current protocol is wrong. Rather, I am wondering
what the consequences are if the protocol is wrong. I have offered a brief
theory where the current protocol could be detrimental to my daughter's
development. There are a couple of truths that were presented above: her
chemical sensitivity is variable, over ten months she has shown constant
improvement. When the injury was speculated to be a stroke I was told that
this was an extremely rare injury because it was so specific to nerves
controlling the diaphragms. Next I was told that the nature of her recovery
was also extremely rare because she was recovering well after strokes resolve/
What I am looking for from the internet is either confidence in the existing
protocol or speculation of possible alternate approaches. I am grateful for
any responses, either to this newsgroup or to me directly.
Finally, I am posting this message because I posted previous messages
promising a follow up. This is not the best follow up I could have written;
it rambles too much. People are welcome to use this information for their
own research or interest, and I will supply additional information if
requested. To all those who have responded in the past: thank you very much.
| PORTERT at sask.usask.ca Tom G. Porter |
| (306)-242-8031 Department of Agricultural Economics |
| In Case of Emergency: Break Glass |
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