X-Message-Number: 2631
Date: 05 Mar 94 02:36:05 EST
From: Mike Darwin <>
Subject: SCI.CRYONICS BPI Tech Brief #3
BPI TECH BRIEF #3
A POSSIBLE ORIGIN FOR THE BURR HOLE DRAINAGE PHENOMENON
Steven B. Harris, M.D. and Michael G. Darwin
This article is not about the last moments of Alexander Hamilton.
A "burr-hole" is a standard medical term for a small window in the
skull made by a surgeon. Such a "craniotomy" or skull penetrating
surgery is today routinely performed on cryonics patients in order to
evaluate the adequacy of blood washout/cerebral perfusion, and
ascertain the development of cerebral edema in a timely fashion during
cryoprotective perfusion. It has historically been very useful for
this purpose, but has had a side effect which is our subject.
A typical burr-hole used to assess a cryonics patient is circular
window in bone some 5-10 mm (1/5 to 2/5 inches) in diameter, and it is
opened near the midline over the parietal or frontal cortex of the
brain soon after the patient has been brought to the operating table
for cryoprotective perfusion. This happens some 3 to 12 hours,
typically, after legal death has been pronounced, depending on
transportation time from the area of the U.S. in which the clinical
death of the patient occurred. The usual procedure for a burr hole is
to incise the scalp in the top of the head with a #10 scalpel blade,
making an incision 3-5 cm in length. The "periosteum" tissue covering
the bone of the skill is then incised with the scalpel and reflected
with a periosteal elevator. Craniotomy or penetration of the skull is
then carried out using either a pneumatic perforator or a Hudson brace
with Cushing burr (a manual drill much like a standard hand wood
drill).
This procedure, surprisingly, is relatively simple to do without
injury to the brain. Next, the "dura mater," which is the thickest
and toughest ("durable") of the layers of tissue protecting the brain
and spinal cord, and the one which is outermost, is opened. For this,
one usually uses a dura hook to retract the dura away from the brain
so that it is not cut when incised with sharp tip of a #11 scalpel
blade. The dura flaps are then trimmed away to the margins of the
opening in the bone.
This procedure was first implemented in January of 1980 on a
patient prepared for Trans Time, Inc. by Cryovita Laboratories
(Cryonics (6(11), 13 (Nov., 1985). The procedure allowed for good
visualization of the pial vessels (vessels in the pia mater, the thin
membrane next to the brain tissue itself). It also allowed good
observation of the degree of blood washout of these vessels in a
patient that had been subjected to air transport packed in ice in the
absence of total body washout (i.e. with blood still present in the
body). Subsequently this technique has been used on all patients
subjected to cryoprotective perfusion by the Alcor Foundation and has
been employed also more recently by Biopreservation. It has proven
very useful in indirectly evaluating the degree of cerebral capillary
integrity.
In patients transported under optimum conditions, with minimal
near death "agonal" ischemic insult due to shock (in this context
tissue underperfusion), the patient's brain typically becomes
dehydrated in response to glycerolization, and remains dehydrated
throughout the course of cryoprotective perfusion, with brain volume
losses of 30 to 50% of baseline volume being common by the termination
of perfusion as estimated by measuring retraction of the cerebral
hemispheres. By contrast, cryonics patients with severe pre-perfusion
ischemic injury (typically caused by a delay between clinical death
and when access to the patient was permitted to cryonicists) either do
not exhibit cerebral dehydration and shrinkage, or else they exhibit
it transiently, followed by the development of progressive and massive
cerebral edema. Perfusion is usually terminated when the brain begins
to herniate (bulge) significantly into the burr opening. In
cryopreservations performed where pronouncement of death is timely and
access to the arrested patient almost immediate, edema typically does
not force termination of perfusion. In perfusion of patients
suffering long periods of ischemia before access was permitted, brain
edema as monitored by the burr-hole has typically forced termination
of perfusion.
A puzzling phenomenon which has been observed fairly consistently
in patients who have exhibited marked cerebral dehydration during
glycerolization (i.e., those thought to have the least brain insult
and the best suspensions), is the leakage during cryoprotective
perfusion of comparatively large flows of perfusate from the
craniotomy opening, usually in the amount of 150 to 250 cc/min. It
has been assumed until recently that all of this leakage was from the
incised bone, scalp and dura. Since these tissues are normally cut
following blood washout, normal intraoperative hemostasis would not be
expected to occur (with no blood there is no clotting).
Over the course of the years one of us (M.G.D.) has made a
number of efforts to control this leakage as well as determine its
source. This was something of a priority, since the loss of this
volume of perfusate from the recirculating system, particularly in the
case of neuropreservation patients, constitutes a volume roughly equal
to that typically withdrawn (and added) to achieve the linear increase
in glycerol concentration in the recirculating perfusate. In
neuropreservations it also constitutes a significant fraction of the
total recirculating and concentrate perfusate volumes over the course
of a typical 2-3 hour cryoprotective perfusion. Additionally, unless
this perfusate is recovered and returned via cardiotomy suction to the
recirculating system, it constitutes not only a hard to quantify
"unknown" affecting the rate of glycerol concentration increase, but
also a significant housekeeping problem as the perfusate is lost to
the table top where it can saturate drapes and complicate operating
room and patient clean-up following the perfusion (this is of
particular concern in patients with hepatitis, HIV or other infectious
blood borne disease).
Early efforts at fluid loss control consisted of using bone wax
to secure hemostasis in bone cortex, and the use of clips and cautery
to stop leakage from the scalp and dura. None of these efforts was
successful, and so it became increasingly apparent that the source of
the leakage was intracranial, excluding the dura. What was not clear
was where this flow was coming from. Did this leakage represent
transudation (direct pressure leakage) from the pia-- the delicate
membrane covering the brain? Or did it come from perivascular spaces,
having leaked from vessels? Was damage to the choroid plexus, the
normal source of cerebrospinal fluid, the source?
None of these explanations seemed probable. Transudation and
increased capillary permeability seemed more likely events in patients
with greater rather than less ischemic injury, yet little that was
consistent with this was noted. In fact, drainage from the burr hole
was routinely highest in patients transported under good conditions
and with maximum amounts of cerebral dehydration! By contrast,
patients with poor cerebral perfusion who did not develop cerebral
dehydration, or who developed only modest dehydration followed by a
rebound to cerebral edema, exhibited little or no burr hole drainage.
None of these facts fit very well. Also, there seemed little reason
why transudation, primarily expected to be a subarachnoid problem,
would show up in the subdural space even before the arachnoid was
damaged.
During the recent cryopreservation of American Cryonics Society
patient ACS 9577, these troublesome problems were illustrated well.
Once more, an attempt was made by M.G.D. to determine the source of
the craniotomy drainage. The scalp and periosteum were incised as
usual and the bone was perforated using a DePuy pneumatic perforator.
However, the dura was not opened at the start of cryoprotective
perfusion. Rather, cryoprotective perfusion was commenced and
perfusate leakage from the scalp and bone were evaluated and
determined to be no more than 10-15 cc/min. Before the start of
perfusion the dura was gently depressed with a probe and was found to
be flaccid with the cerebral cortex not palpable at a depression of 1-
2mm. The pressure of fluid in the subdural space was obviously not
high.
Approximately 30 minutes after the start of perfusion the dura
was again depressed and was found to be moderately tense. Fluid
apparently had begun to accumulate in the subdural space between the
outer membrane protecting the brain (the dura), and the arachnoid
membrane beneath, even though the outer membrane was at that point
intact and there were no cuts as yet beneath to leak from. Seventy-
three minutes into cryoprotective perfusion the dura was pierced with
a 16 gauge needle and a copious, moderately high pressure flow of
clear fluid was observed to issue from the needle. At this point the
needle was withdrawn and the puncture in the dura was widened with a
#11 scalpel blade approximately 1 mm in diameter. A copious and
pressured flow of fluid was observed streaming from the puncture.
The flow rate of fluid out of the puncture in the dura was
measured by collection in a graduate over a 1-minute period and was
found to be 150 cc/min. A nearly maximal fluid leak was occurring in
deeper layers of the brain, obviously independently of surgical
trauma.
The opening in the dura was then widened and a probe was passed
to determine the degree of cerebral dehydration . The
cortical/arachnoid surface was determined to be 7 mm below the inner
surface of the cranial vault. A length of plastic tubing was then
passed into the craniotomy such that flow from the dura, bone and
scalp were excluded. Flow of fluid from the cranial vault was
measured at approximately 140 cc/min. This fluid was then evaluated
for cryoprotective agent concentration and for blood gases and
electrolytes. The character of this drainage was venous in nature.
This fact agrees with previously measured concentration of glycerol in
burr hole drainage in both published (Cryonics 1986 Feb;7(2):15-32)
and unpublished Alcor cryopreservation case histories A-1133 and A-
1169 in which burr hole glycerol concentration as measured by
refractive index was found to overlap the measured glycerol
concentration in the patient's venous (as opposed to arterial)
circulation.
Possible Sources of Intracranial Fluid
The determination of the character of this drainage as primarily
of venous origin deep to the dura and independent of surgical trauma,
taken with consideration of the anatomy of the meninges, suggests
three possible sources, any of which may operate alone, or any
combination of which may operate together.
The most likely possibility is fluid leakage from tears or
ruptures in the bridging veins between the dura and the next innermost
membrane (the arachnoid), as a result of shrinkage of the cerebral
hemispheres in response to glycerolization. A second possibility is
that shrinkage of the brain may partly separate the two layers of the
dura mater (the endosteal which lines the inside of the skull and the
meningeal layer which is deep to this, thereby disrupting one or more
the large venous sinsuses which run between these layers in many parts
of the skull, and which are not even properly vessels. It is even
possible that some past burr holes, perhaps placed too near the
midline, have penetrated the endosteal layer of dura only to open into
the large sagital venous sinus which runs down the midline at the top
of the skull. When not filled with blood such a sinus would appear
only as one more potential space in the skull. A third and final
possibility is that loss of competency in the microscopic valves of
the arachnoidal villi has occurred as a result of glycerol-induced
dehydration of the endothelial cells which cover the villi, and which
normally regulate the flow of cerebrospinal fluid into the venous
blood.
Localized injury to bridging veins from deceleration injury is a
known source of intracranial venous bleeding and is a common cause of
subdural hematoma, which results often from venous leakage into the
subdural space. This phenomenon has also been well described in
nontraumatized patients receiving mannitol, an osmotic and dehydrating
agent, during heart bypass (Surg Neurol 1985 Nov;24(5):520-524).
Cryonics perfusate contains both mannitol and glycerol in large
quantities. The pronounced cerebral dehydration which occurs as a
consequence of the perfusion of osmotically active agents during
cryoprotectant perfusion necessarily results in separation of the
arachnoid membrane from the dura (the dura remains adherent to the
inside of the cranial vault) and presumably could also result in
tearing of the bridging veins which connect the dura and the arachnoid
membrane. Hypothermia may contribute to reduced elasticity in such
veins, and lack of hemostasis and clotting insures that if there is a
rupture, it will leak fluid copiously and continuously.
A second source of the fluid leak might be the superior sagital
venous sinus, or one of several other venous sinuses which might
potentially be disrupted by brain dehydration and separation of the
two layers of dura which form them. More care will be required in the
future to place burr-holes off midline, and to attempt to identify
both layers of dura when dura is being penetrated.
A third fluid source might (though implausibly) be the arachnoidal
villi. The arachnoidal villi are microscopic projections of the
arachnoidal membrane through the walls of the venous sinuses (large
venous reservoirs which collect blood from brain flow). Electron
microscopy of the endothelial cells covering these projections
discloses the presence of large vesicular holes which pass through the
body of the cells. These holes or pores are large enough to allow for
the relatively free passage of the cerebrospinal fluid (CSF) into the
venous blood, and may be large enough to allow for even the passage of
some formed elements such red blood cells (Guyton AC, Textbook of
Medical Physiology, W.B. Saunders, Philadelphia, 1991: 682-683.).
Under normal physiologic conditions the arachnoidal villi act to
reabsorb CSF when the pressure of the CSF is about 1.5 mm Hg greater
than the pressure in the venous sinuses. Normally the amount of CSF
absorbed during the course of a day by this mechanism is modest, in
the range of 150 to 200 cc. The effect of osmotically active
compounds such as glycerol, dimethylsulfoxide or other cryoprotective
compounds on the cellular "valving" mechanism in the arachnoid villi
is unknown. However, the possibility exists that cellular dehydration
may greatly increase the size of the pores in the villi cells
resulting in a leakage of venous effluent retrograde from its normal
path, from the venous sinuses into the subarachnoid space.
Ordinarily the subarachnoid space in the brain does not
communicate with the subdural space above it, so that in the absence
of an arachnoid membrane tear, a fluid leak in the subarachnoid space
seems less likely to show up as a spontaneous and rapid subdural (not
subarachnoid) fluid collection, which examination of the most recent
suspension strongly suggested was the primary problem.
Significance of The Problem
While this kind of injury would be of great concern under
physiologic conditions it is of significance to the cryopreservation
patient only if a burr-hole is *not* opened in the skull. In such a
situation the accumulation of venous perfusate at venous pressure
might significantly reduced brain perfusion, in effect creating a
large bilateral subdural hematoma.
Determining The Source of The Fluid
In subsequent cases where ischemic time is minimal and brain
perfusion is good (with associated cerebral dehydration) we will
undertake to definitively determine the source of the leakage. If we
can identify the subarachnoid space during cryoprotective perfusion we
will attempt to pass a needle into it to obtain some (subarachnoid)
CSF. If this is still chemically very different from venous return
(and it should be in every scenario except the leaky villi one), then
we can be fairly confident that the source of the leakage is subdural
either from injury to bridging veins or torn venous sinuses.
ABSTRACTS OF INTEREST DOCUMENTING DEHYDRATION AS A SOURCE OF SUBDURAL
HEMATOMA SBSEQUENT TO BRIDGING VEIN INJURY:
AU - Giamundo A ; Benvenuti D ; Lavano A ; D'Andrea F
TI - Chronic subdural haematoma after spinal anaesthesia. Case report.
AB - In this study an interesting and not frequent case of
non-traumatic chronic subdural haematoma after spinal anaesthesia
is reported. After a careful review of the cases described in the
literature, the Authors discussed the physiopathological
mechanisms, emphasizing how the break of the bridge veins or of
the subarachnoid granulations, the cerebral atrophy and the
dehydration are factors which facilitate the appearance of this
neurological complication. They suggest that a suitable
post-operative rehydration is an important prevention factor.
SO - J Neurosurg Sci 1985 Apr-Jun;29(2):153-5
AU - Yokote H ; Itakura T ; Funahashi K ; Kamei I ; Hayashi S ; Komai N
TI - Chronic subdural hematoma after open heart surgery.
AB - Three cases of chronic subdural hematoma after open heart surgery
are reported. In all cases, computed tomography scans revealed
subdural accumulations of high density after cardiac surgery. The
high-density areas changed into isodensity or low density with
mass effect within 2 or 3 weeks. Anticoagulant (heparin) and a
tearing of bridging veins after a rapid change of the brain
volume by administration of mannitol can be a cause of chronic
subdural hematoma. Forty-five to 60 mL of liquefied hematoma was
aspirated and the outer membrane of the hematoma cavity was
recognized by a trepanation.
SO - Surg Neurol 1985 Nov;24(5):520-4
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