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Permissive Hypotension in TBI [was Prehospital Fluid]

Karim Brohi karim at trauma.org
Mon Apr 9 12:24:03 BST 2012

This practice of relaxing permissive hypotensive strategies in the
presence of a head injury is common but is more emotional than data
driven.  There are very few studies that explore this area but the few
that do don't support it.

The best one I have seen that explains this is admittedly a pig study
from 1998 (abstract below).  This shows that there are two halves to
the CPP equation (CPP = MAP - ICP -CVP).

We assume that volume = higher MAP = improved CPP for a given ICP.
However if volume = increased cerebral oedema = higher ICP then it
depends whether the MAP increase is greater than the ICP increase.  In
pigs anyway, early resuscitation is associated with increased ICP,
decreased CPP and decreased Cerebral Blood Flow.  There is also of
course the potential to exacerbate a dilutional coagulopathy leading
to an exacerbation of the brain injury.

There's a good rat study as well which also shows that treatments to
push pressure up lead to decreased survival and functional outcomes in
TBI with uncontrolled haemorrhage (also below).  Most importantly in
this paper, every rat given a vasopressor died.

Anyway - there are no quality human studies here (again partly due to
the emotion involved).  But the decision-making here is far from clear
cut.  [If anyone knows of a reasonable human study please let me/us


Arch Surg. 1998 Apr;133(4):390-8.
Delayed fluid resuscitation of head injury and uncontrolled hemorrhagic shock.
Bourguignon PR, Shackford SR, Shiffer C, Nichols P, Nees AV.
Department of Surgery, University of Vermont College of Medicine,
Burlington 05401, USA.
To evaluate the effects of delayed vs early fluid resuscitation on
cerebral hemodynamics after severe head injury and uncontrolled
hemorrhagic shock.
Prospective, randomized, controlled experimental trial.
Surgical research laboratory.
Immature swine (N=16) weighing 40 to 50 kg.
Twelve swine were subjected to cryogenic brain lesion and hemorrhage
to maintain a mean arterial pressure (MAP) of 50 mm Hg. Animals were
randomized to receive 1 L of Ringer lactate solution in 20 minutes,
starting 20 minutes after injury and hemorrhage, followed by 1 L of
Ringer lactate solution in 30 minutes (ER group) (n=6), or no fluid
resuscitation (DR group) (n=6). The 4 control animals underwent
instrumentation only. The study ended 70 minutes after head injury and
Measurements of MAP, bilateral regional cerebral blood flow, serum
hemoglobin level, systemic and regional cerebral oxygen delivery, and
intracranial pressure performed at baseline and 20 (phase 1), 50
(phase 2), and 70 minutes (phase 3) after head injury and hemorrhage.
Lesion size (percentage of ipsilateral cortex) was measured post
All animals survived the experimental period. Systemic cerebral oxygen
delivery in the DR group was significantly lower at phase 3 compared
with that of the ER group (31.5% vs 53.1% at baseline) (P=.03).
However, bilateral regional cerebral oxygen delivery was significantly
greater in the DR group at phase 3 compared with that of the ER group
(71.5% vs 47.0% at baseline in the injured side; 72.9% vs 48.4% at
baseline in the noninjured side) (P=.02). Bilateral cerebral blood
flow was similar in all groups at all times. The ER group showed a
trend toward a greater intracranial pressure elevation (6.8 vs -0.25)
(P=.07) and lesion size (37.0% vs 28.6%) (P=.07). Hemoglobin level
became significantly lower in the ER group at phase 2 (7.0 vs 10.7)
(P=.03) and remained lower at phase 3 (6.9 vs 11.7) (P=.01).
Early fluid resuscitation with Ringer lactate solution following head
injury and uncontrolled hemorrhagic shock worsens cerebral
hemodynamics. Cerebral pressure autoregulation is sufficiently intact
following head injury to maintain regional cerebral oxygen delivery
without asanguineous fluid resuscitation.

Anesth Analg. 1999 Oct;89(4):950-6.
Treatments to support blood pressure increases bleeding and/or
decreases survival in a rat model of closed head trauma combined with
uncontrolled hemorrhage.
Talmor D, Merkind V, Artru AA, Shapiro O, Geva D, Roytblat L, Shapira Y.
Division of Anesthesiology, Ben-Gurion University of the Negev,
Faculty of Health Sciences, Soroka Medical Center, Beer Sheva, Israel.
Hemorrhagic hypotension may aggravate the detrimental effects of head
trauma on neurologic outcome. Our study examined whether using
phenylephrine or large volumes of saline IV to increase mean arterial
blood pressure (MAP) to 70, 80, or 90 mm Hg during the combination of
head trauma and uncontrolled hemorrhage would improve neurologic
outcome. Rats were assigned to one of 17 groups. In Groups 1-5, the
variables were head trauma (yes/no), hemorrhage (yes/no), 0 or 3 mL
saline per milliliter of blood lost, and no target MAP. In Groups
6-11, hemorrhage was or was not combined with head trauma, and large
volumes of saline were given IV to achieve target MAPs of 70, 80, or
90 mm Hg. Groups 12-17 were similar to Groups 6-11 except that
phenylephrine was used rather than saline to achieve target MAPs.
Saline increased blood loss at 2 h to approximately 16 and 25 mL at a
MAP of 80 and 90 mm Hg respectively, increased (worsened) the
neurodeficit score but not cerebral edema at 24 h, and decreased
survival rate at 2 and 24 h. Because phenylephrine was fatal for 62 of
63 rats, group mean values for blood loss, neurodeficit score, and
brain tissue specific gravity could not be calculated. We conclude
that supporting MAP with either phenylephrine or large volumes of
saline worsened the neurodeficit score and/or survival and did not
affect cerebral edema formation in our rat model of head trauma
combined with hemorrhage. IMPLICATIONS: The results of this study
indicate that maintaining mean arterial blood pressure at 70, 80, or
90 mm Hg with either phenylephrine or large volumes of saline worsened
the neurodeficit score and/or survival and did not affect cerebral
edema formation in our rat model of head trauma combined with

On Sat, Apr 7, 2012 at 17:46, Garth Melnick <gmelnick at efn.org> wrote:
> Hi all,
> I know, I know, this is a very dead horse. But I have a slightly different
> angle on it this morning.
> I'm an ambulance paramedic; I also work on a small team providing wilderness
> ALS care. Often we have prolonged evac / transport times. I recently ran
> across the recommendations of the International Commission for Mountain
> Rescue on fluid resuscitation.
> They're here: http://bit.ly/HSPa56
> Interestingly, in the setting of PROLONGED prehospital time and a patient
> with suspected TBI (GCS <9), this committee recommends resuscitating pts to
>>110mmHg for cerebral perfusion. Otherwise the target is 90mmHg. They note
> pts with suspected ongoing hemorrhage should be maintained at a lower SBP.
> I'm curious what the experts here think. I know the consensus is restricted
> fluids prehospital and a target SBP of 90mmHg. How does a serious TBI change
> that? How does a 6 hour – or 24 hour – prehospital time change that?
> Thanks,
> Garth
> --
> trauma-list : TRAUMA.ORG
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