Transcript Case-Based Presentation: Trauma

Case-Based Presentation: Trauma
CCM Academic Half-Day
11 December 2008
Case #1: Don’t mind your own
business, whatever you do…
• You are moonlighting in the emergency
department in a very, very rural hospital and field
a base contact call from a paramedic crew.
•
A young man minding his own business in a
bar was shot several times with a handgun,
according to witnesses. His GCS is E2 V3 M 4,
with rapid, weak pulses. His vital signs: HR 130,
RR 28, BP 110/65. Primary survey reveals two
penetrating wounds to his chest and one hole in
his abdomen. There are no other reported injuries.
• The paramedics called for a helicopter for direct
transport to Vancouver, but it will take about an
hour to reach them, as the sole functioning
machine is being refueled. Your hospital is
approximately 50 km from the scene, with a
parking lot that would serve nicely as a helipad.
– The paramedics are seeking some wisdom…
• What is the current evidence regarding out-ofhospital trauma life support?
• What should the destination be for this patient?
In the ED
• He remains resistant to attempts to immobilize
him, and makes a mockery of spinal precautions.
The ambulance crew delivers him to your
resuscitation bay with a GCS 9, with a heart rate
of 150 and BP 100/60. RR is 30. He has a patent
airway, quiet breath sounds bilaterally, penetrating
injuries as described, a tender, firm abdomen and
is moving all extremities. His skin is pale and
diaphoretic.
Immediate Management Goals?
A little assistance, please…
• The trauma service at VGH is an hour away
including helicopter response time. A
general surgeon is on call at your hospital,
and he may still be rounding. He’s not
Naisan. Would you refer him to the
immediately available service, or call for a
helicopter? Why?
Case # 2: Deere Me
• The following week, at VGH…
• A truck carrying a riding lawnmower on the
freeway dropped its payload and the wayward
John Deere struck a midsize car following at 100
kph. The car then careened into the center divide
and rolled several times before coming to rest in a
ditch. The driver (Unknown A), a 30 year old man,
was trapped in the car for 30 minutes. He was
intubated in the car, then extricated after the roof
was sawn off. Initial GCS was 6 (E1 V1 M4).
AC 1
• Now he is in full spinal immobilization, intubated
and mechanically ventilated. GCS is E1, V(T), M
1. Vital signs are HR 140, BP 100/50, RR 12 on
ACV. SPO2 is 92% on FiO2 0.35. Pupils are
unequal ( R 3 mm and reactive, L 6 mm and
fixed). An abraded area on his forehead and an
obviously fractured left clavicle are his only
immediately apparent external injuries.
– Neurosurgery has arrived, and the resident has managed
to coax the radiology resident into approving a stat CT
brain, but “you have to send the patient right now!”
AC 1
• What are the immediate concerns regarding
his hemodynamic mangement in light of his
neurologic injury?
• What will you do about it?
Main Goal
• Current exam suggests severe TBI with
possibility of uncal herniation (blown pupil)
• His BP is 100/50, sats 92%
• Hypotension (SBP<90mmHg) and hypoxia
(sats <90%) must be avoided as they are
independent risk for mortality and
morbidity.
– Traumatic Coma DataBase: Single episode of
hypotension from injury through resus is
associated with doubling of mortality and
similar increase in morbidity!.
Specific Management
• Need to decrease pressure in the head
acutely.
• Try to maintain oxygenation and CPP.
– Place on 100% O2
– Hyperventilation to decrease CO2 (25-35
mmHg) to acutely vasoconstrict intracranial
vasculature.
• This is OK for short term but unknown long term
consequences, as it will decrease cerebral blood
flow…
Hyperosmolar Therapy
• Mannitol: widely accepted use to acutely
treat severe increased ICP
– Immediate plasma expanding effects cause
decreased hematocrit, decreased viscosity,
which increased CBF and O2 delivery
– Osmotic effect delayed 15-30 min, be careful in
hypotension!
– May also increase risk of renal failure
The RT appears, as if from
nowhere…
• Any particular ventilation strategy for this
patient?
– 100% O2
– Stat ABG and hyperventilate as above.
– Careful with PEEP (may exacerbate
hypotension, with possible increase in ICP)
– Follow patient to CT scanner
• Hypertonic saline: mechanism of action likely:
– Osmotic action to decrease cerebral water content
– Dehydrates endothelial cells and RBCs leads to
increased diameter of vessels and deformability of
RBC-better blood flow
– Also reduces leukocyte adhesion in traumatized brain
– Watch out in chronic hyponatremics!
CT Brain
• The CT shows subarachnoid blood, a right
temporal subdural hematoma (8 mm) and
surrounding edema with midline shift and
uncal herniation.
– Clinical correlation is required.
QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
• An EVD is placed, with initial intracranial
pressure measuring 40 cm H2O.
• The patient appears in the ICU, and the
bedside nurse insists upon orders right this
very second, as the neurosurgery post-op
orders are illegible without the Rosetta
Stone.
Orders, please.
• MAP goals?
• What about the EVD?
• Nimodipine for traumatic SAH with
hypotension?
• Should we start phenytoin?
• Where did you leave your coffee?!
Next time, just let the coffee mug
go…
• Unknown B is a 50 year-old woman with an
unknown medical history. She was encountered 15
feet from the stopped car, and was initially
unresponsive with strong pulses and spontaneous,
snoring respirations. She now has an oral airway
in place, is in full spinal precautions and has the
following vital signs: HR 100, BP 100/40, RR 8,
SpO2 92% on oxygen by face mask. You perform
the primary survey, as you happen to be standing
closest to the ER stretcher.
“What are my MAP goals?”
• Autoregulation:
– CBF remains stable despite
rise and fall in CPP
• With severe TBI, autoregulatory
function is compromised
–  CPP can lead to CBF
– Might need a higher CPP to
avoid ischemia
Avoid secondary insult
• Single episode of hypotension during
resuscitation  double mortality
• Recommend SBP > 90 during initial
resuscitation
• Recommendation from European guidelines
MAP>90.
Br J Anaesth 2007; 99: 18-31
Avoid Secondary insult
• Brain Trauma Foundation:
– Aggressive attempts to maintain CPP above 70
mm Hg with fluids and pressors should be
avoided due to increase incidence of ARDS
(Level II)
– CPP of 50 mm Hg should be avoided. (Level
III)
Management of ICP
• Goal of balancing risk of herniation with
risk of over treatment
• No large RCT comparing different levels of
ICP targets
• Brain Trauma Foundation recommend:
– Maintain ICP < 20mmHg (level II evidence)
aSAH
• HHH therapy: hypervolemia, HTN, hemodilution
• First reported in 1976
• Incidence of delayed ischemia  by 50%
Nimodipine and SAH
• Goal is to avoid secondary ischemia
• Delayed cerebral ischemia due to
vasospasm is the most common cause of
death and disability in aSAH
• Nimodipine treatment didn't influence
presence of angiographic vasospasm
– benefit linked to cytoprotective rather than its
vasodilatory properties?
Nimodipine and SAH
• Cochrane review 2007 for aneurysmal
SAH:
– Nimodipine reduced risk of poor outcome
and
(RR was 0.67 (95% CI 0.55 to 0.81))
– IV nimodipine not recommended
– Recommend nimodipine 60mg PO Q4H for 3
wks
– Can give 30mg PO Q2H if BP low.
Nimodipine and TBI
• Cochrane Review of CCB in TBI 2003:
– No benefit of CCB in TBI patients
– Subgroup analysis for traumatic SAH for risk
of death from 2 RCTs
• pooled OR 0.59 (95% CI 0.37 to 0.94).
– Higher risk of hypotension in CCB group.
Unknown B
• GCS is E2 V2 M1. She coughs against the
oral airway, and there are no secretions nor
blood noted in her mouth. There is some
blood on the backboard beneath her occiput.
No chest nor abdominal abnormalities are
noted. She does not move her extremities,
and her skin is warm with normal capillary
refill.
Radiological adjuncts
• How would you manage her airway?
• What imaging is necessary before a
treatment plan can be made?
– How good are CT and MRI at determining the
nature of vertebral and spinal cord injuries?
• CT brain shows suggestion of cerebral edema, but
no midline shift nor evidence of uncal/tonsilar
herniation. There is a C4 body and facet fracture
with fragments projecting into the canal. CT
angiography reveals a right cervical carotid
dissection, just outside the skull. There is flow on
either side. Spinous process fractures are noted at
T 10 and 11. The lumbar spine is unremarkable.
• The patient is now in the ICU, with GCS E2
V(T) M1. HR is now 115 and BP is 90/40,
giving her the highest unsupported MAP in
the unit. The spine service is occupied in the
OR, but plan to operate on her as soon as
the room is turned over.
• What is the strategy for managing her
hemodynamics?
Approach to hemodynamics in
TBI
• Although the imaging is not as spectacularly abnormal as
in Unknown A, the guidelines defined by the Brain Trauma
Foundation still apply
– SBP <90 mmHg should be avoided.
• In hospital, a single episode in pts w/ a GCS < 13 showed a
trend toward incr mortality, while two or more episodes
carried a relative risk of 8.1.
• Increased duration of hypotension is also assoc w/ incr
morbidity and mortality.
Approach to hemodynamics in
TBI
• The optimal choice of resuscitation fluid has yet to be
defined, although there is some evidence that hypertonic
saline is superior to Ringer’s lactate (improved survival). I
would not use albumin in this patient, given the increased
mortality for trauma pts seen in the SAFE trial (especially
brain injured pts; (relative risk, 1.62; 95% CI, 1.12–2.34).
• The optimal BP has yet to be defined, although significant
guidelines suggest a goal MAP > 80 or 90, which more
closely correlates with CPP.
• There is insufficient evidence at present to suggest which if
any vasoactive agents should be used to support arterial
pressure if fluids alone are inadequate.
Dr. Mountain’s consult note
• So, to answer the question, I would volume
resuscitate with blood if necessary based on her
Hgb, and any active bleeding. Once bleeding and
Hgb were stable, I would continue to support her
pressure to a MAP > 80 with NS, and then
probably levophed if necessary.
• I would aggressively avoid episodes of
hypotension, and if any happened inadvertently, I
would correct them as quickly as possible, and
yell expletives I learned from Naisan at the
responsible resident.
Is there a role for steroids in her
management?
• No.
Details?
• In the 60s and early 70s, steroids were commonly given to
TBI pts on the basis of their beneficial effect on brain
tumor pts, and some early studies suggesting positive
effects in TBI.
• Since the mid-70s, multiple studies and a meta-analysis
have shown no benefit of steroids in TBI.
• In addition, one study has shown an increased risk of first
late seizures in pts treated with steroids, and a large study
(10,008 pts) in 2004 was stopped early due to incr
mortality in TBI pts treated with methylpred (RR 1.18,
95% CI 1.09-1.27, p = 0.0001).
• TF, the Brain Trauma Foundation guidelines
state that the majority of evidence indicates
that steroids do not improve outcome or
lower ICP in severe TBI. There is strong
evidence that steroids are deleterious; thus
their use is not recommended in TBI.
“Should an EVD be placed?”
• …asks the pathology resident. “They put
one in the other guy…”
Endoventricular Drain
• The BTF states that Level II evidence supports the
placement of an ICP monitoring device in all salvageable
patients with a severe TBI (GCS 3-8 after resuscitation)
and an abnormal CT scan (hematomas, contusions,
swelling, herniation, or compressed basal cisterns).
• ICP monitoring should be done with a normal CT scan if
two or more of the following at admission: age > 40, any
motor posturing (unilateral or bilateral), or SBP < 90.
• These factors define pts at high risk for ICH (53-63%).
• With a normal admission scan, the risk is about 10-15%
(followup scanning necessary).
• TF, the BTF recommends the use of ICP
monitoring in pts at risk for ICH, to more
accurately allow measurement of CPP, and
therefore appropriate treatment, earlier detection
of ICH, and treatment via CSF drainage.
• They note that ICP cannot be reliably predicted
from CT scan alone, that ICP data are useful in
predicting outcome and guiding therapy, and that
not monitoring ICP while treating for ICH can
result in deleterious outcomes.
• In this patient, there is a suggestion of cerebral
edema on her CT scan, which would qualify as
abnormal according to the BTF.
• Even if it was not abnormal, the fact that she is
over 40, and she has absent motor responses on
her GCS suggest that she is at high risk for ICH,
and her ICP should be monitored, and treatment
tailored to the readings.
• Nice job pathology resident!
“And the carotid is dissecting. Uhh, is
there something we’re supposed to be
doing about that?”
•
•
•
•
Incidence in blunt trauma is 1%
Thromboemboli
Stenosis
Occlusion
Treatment options
• Antiplatelets
• Anticoagulants
• Stents/angioplasty
• Considerations in Trauma
Cochrane review
• No RCT’s
• No difference between anticoags and
antiplatelets for death and disability
Do they heal?
• 90% heal in 3-6 months
• 50% recanalize from complete occlusion
Back to Unknown A
• As the patient is rolled to the OR, you are paged
about Unknown A, whose name has since become
available but nobody can remember it. In the
course of performing his physical exam, the
resident noted that the patient’s left pupil is the
same size it was in the ER, although it was
documented to be 4 mm and reactive following
EVD placement. He is breathing
dyssynchronously with the ventilator. “What do
we do? There’s already a drain in place!”
Yikes
• What do we do? There’s already a drain in
place?
• Is there a role for hypothermia here?
• Would any other monitoring modalities be
useful here?
What do you do? There’s already a
drain in place!
• Treatment to decrease ICP
–
–
–
–
Mannitol
3% saline
Hyperventilation
Surgical decompression
• Treatment to decrease CMO2
– Sedation
– Mechanical ventilation
– Normothermia
Please comment on the role of
hypothermia in managing elevated
intracranial pressure.
It should work
• reduction in brain metabolic rate
• effects on cerebral blood flow
• reduction of the critical threshold for oxygen
delivery, blockade of excitotoxic mechanisms
• calcium antagonism
• preservation of protein synthesis
• reduction of brain thermopoolin
• a decrease in edema formation
• modulation of the inflammatory response
• neuroprotection of the white matter
• modulation of apoptotic cell death.
It does work…..
• Animal studies are encouraging
• Appears to help in post cardiac arrest
cerebral anoxia
• Some human studies in TBI appear to show
a benefit
• BUT …………….
The breadth of the evidence is
equivocal
Part of it is encouraging
TBI guidelines
Some people are not giving up on
Hypothermia
• Surface cooling
• Intranasal selective hypothermia
• Transarterial or transvenous endovascular
cooling
• Extraluminal vascular cooling
• Epidural cerebral cooling.
Time to meet the family
• Does he have brain damage?
• Is he going to get any better than this?!
• Should we start planning for discharge?
Primary vs Secondary Brain
Injury
• Primary injury: experienced at the moment of
traumatic incident.
– There is NOTHING to be done about the primary
injury!
• Secondary injury: caused by ischemia (hence the
need to avoid hypotension and hypoxia) and the
sequelae of deranged intracranial pressure.
– This is the opportunity to salvage neurologic function!
Prognostication
• Extremely difficult in patients who are
initially comatose or who require sedation
to allow for ongoing care.
• Data are suboptimal in terms of study
design, definitions and timelines.
• As a result, exact percentages are nearly
impossible to provide.
Glasgow Coma Scale
• GCS at first assessment (i.e. immediately
post-injury): GCS 3 is associated with 80%
mortality and approx. 10% functional
neurologic survival across all studies.
• Note wide variation in time of “initial” GCS, from <
6 hrs to 7 days.
• Age > 60 yrs, not accounted for solely by
medical comorbidity (i.e. inherent loss of
ability of older brain to heal).
Prognostication
• Bilaterally absent pupillary light reflex after
hemodynamic resuscitation.
– Reflex pathway is adjacent to areas responsible
for cognitive function.
– Correlates to approx. 88% dead or vegetative
state.
– Numbers affected by orbital trauma,
hypotension, and hematomas/ subsequent
surgery.
The money…Hypotension
• SBP < 90 mm Hg at any time from injury
through ICU stay!
– Single recording of hypotension during critical
care stay correlates to approxiately double the
mortality!
– This is the most addressable of all the
prognostic signs.
CT Scan Findings
• Basal Cisterns: compression or absence
associated with elevated ICP
• Traumatic subarachnoid hemorrhage
• Midline Shift
• Intracranial mass lesion