This document provides an overview of the approach to brain trauma management in the intensive care unit. It discusses: 1. Using a multidisciplinary team approach and following protocols to consistently provide great care for traumatic brain injury patients. 2. Identifying and treating both primary brain injuries from the initial trauma and secondary injuries that can develop over time through techniques like intracranial pressure monitoring and control, seizure prophylaxis, and infection prevention. 3. Preventing secondary injuries like herniation, edema, and reduced blood flow through careful monitoring, normalization of physiology, and medical or surgical interventions when needed. The goal is to prevent further brain damage after the initial trauma.

1. Approach to Brain
Trauma in the ICU
David B. Seder MD, FCCM, FCCP, FNCS
Pulmonary and Neurological Critical Care
Chief, Maine Medical Center Department
of Critical Care Services
Associate Professor of Medicine – Tufts
University School of Medicine

2. Disclosures
 No financial conflicts
 Clinical neurocritical care, clinical research
 Research funding:
 PCORI CER-1602-34137
 NIH CTR grant through NNE consortium
 Maine Brain Aneurysm Awareness Committee

3. Overview
 Toolbox
 Neuro exam, anatomy, disease-specific knowledge
 Identifying and treating primary and secondary
injuries after brain trauma
 Guidelines – what we should all do
 Test prep – what should you study?
 Cases

4. TBI management
 Team approach
 Neurosurgery, critical care, nursing, rehab
medicine, therapy
 Protocols, algorithms, pathways – deviate
when necessary, but start with the basics!
 Family support
 Goal should be consistently great care

5. Toolbox: Neurological exam
 Elements of a good neuro exam depend on the
patient
 Comatose:
 LOA, cranial nerves, motor x5, reflexes, tone,
movements
 Awake
 Add orientation, speech, cognitive assessment,
memory, strength, affect and behavior, other
 Spinal cord injury:
 Motor and sensory levels, reflexes

6. Toolbox: Neuroanatomy
 Parts of the brain/what they do
 Compartments
 Arterial supply
 Venous drainage
 CSF compartments and flow
 Specific injuries give specific
patterns of injury
 Pattern recognition!

7. Neuroanatomy
 Study
 Look at your
scans
 Get an atlas
and look
things up!

8. Toolbox: Know the diseases!
 Some different pathologies within TBI…
 Brain contusion
 Subdural hematoma
 Epidural hematoma
 Arterial dissection
 Vasospasm
 Stroke
 Diffuse axonal injury
 Different diseases have different courses
 Help family know what to expect
 Allows you to pace yourself, provide the right support

9. Each TBI is unique

10. Different injuries require
different management
 Surgery
 Hematoma evacuation
 Arterial repair
 CSF diversion (shunt, EVD, lumbar drainage)
 Cranial reconstruction
 Seizure medications
 Temperature management
 ICP control…etc.

11. 1. Catalogue the injuries
 Look for hemorrhages
 Consider the mechanism of injury, and look for
trouble
 Dissection, spinal injury, CSF leak?
 Injuries evolve over time – anticipate!
 Edema, hematoma expansion, hydrocephalus, arterial
emboli, venous thrombosis, herniation
 Think of each injury individually, not just “TBI”
 If you don’t look, you may not find…

12. Primary vs. Secondary Injuries
 Primary
 Contusions
 Arterial tears
 Subdural hematomas
 Subarachnoid
hemorrhages
 Concussive (blast)
injuries
 Penetrating injuries
 Secondary
 Biochemical injury
 Seizures/excitotoxity
 Intracranial
hypertension &
ischemia
 Brain herniation
 Infection
 Rebleeding
 Vasospasm
 Stroke

13. 2. Treat the primary injuries
 Early surgical/endovascular procedures to
address
 Mass effect, compression, bleeding, thrombosis
 ICP/PbtO2/metabolic brain monitoring and CSF
drainage
 Bony stabilization and reconstruction
 Relieve ischemia
 Delayed surgery for complications and
prevention of secondary injury

15. Early brain injury management
 Stabilize & transfer/triage
 Surgery – or not
 Normalize physiology
 Oxygen, pH/CO2, glucose, BP/CPP, temperature
 Monitoring
 Family: trust, expectations, immediate needs
 Creating the right treatment milieu – do we
have the right team in place?

16. 3. Prevent, identify, and treat
secondary injuries
 Reverse anticoagulants
 Prevent seizures
 Heparin or antiplatelet therapy for arterial
injuries
 Electrolyte corrections
 Antibiotics…sometimes
 Normalize physiology

17. Prevent…
 Reverse anticoagulants
 Warfarin with PCC, vitamin K, maybe FFP
 DOACs with PCC, targeted therapy
 Involve an expert
 Dosing interval matters – when was the last dose?
 Heparins with protamine sulfate
 Antiplatelet agents with…?
 Platelets, DDAVP, nothing

19. Prevent
 Seizures with AEDs x 7
days
 Often levitiracetam,
phenytoin
 BUT…these drugs are also
associated with worse
cognitive outcomes in a
dose-dependent manner!
 We don’t know what to do
 Alternative is monitor and
treat seizures when they
occur

20. Normalize physiology!
 Deranged physiology worsens secondary injury
at a biochemical level
 Very high levels of oxygen increase oxygen-free
radical production in tissues
 Low levels of oxygen or glucose worsen ischemic
injury
 Very high glucose creates oxidative stress in tissues
and bloodstream
 Hypotension strongly associated with worse
neurological outcomes
 Severe hypertension can worsen edema

21. Identify…
 Look for seizures
 May be nonconvulsive (subtle) – check EEG!
 Consider arterial injuries
 Prevent stroke!
 Consider venous thrombosis
 Low threshold for imaging when the exam
deficits do not match the imaging, or there
is an acute change in the exam

22. Treat…
 Treatments for TBI depend on the individual
physiology
 Some patients may benefit from surgery
 All patients benefit from good ICU care:
 Normalization of physiology
 Frequent accurate exams (identify new problems)
 All families need support and social work
 Mild injuries may not be so mild – rehab is key

23. Herniation syndromes
 1. Subfalcine
 Asymmetric motor posturing
 2. Uncal
 CN 3 palsy, contralateral
motor posturing
 3. Transtentorial
 Coma, symmetric posturing,
rostral-caudal loss of
brainstem reflexes
 4. Posterior fossa
 Cerebellar (up or down)
 Coma, bilateral motor
posturing
J Intensive Care Med 2002;17:55-67

24. “Brain sag”
 72 yo man with
facial fractures after
a fall
 Pneumocephalus
 Neurological
decline due to SDH
 “Not waking up”,
“posturing”
 Woke when placed
in Trendelenberg

25. Outcomes with herniation events
 Survivable, but causes secondary
neurological injury
 Compression of large arteries,
worsening of ischemia where
small vessels are underperfused
 Stretch injury
 Contralateral compression injury
 2008 Hopkins series
 68 patients (76 events) with TTH
treated with 30-60cc 23.4%
saline
 32% survival, 7.4% good neuro
outcome
 17% transient hypotension
 2000 Hopkins series
 28 pts with 32 episodes TTH
 Mannitol
 Intubation/Hyperventilation
 Hypertonic saline
 Barbiturates
 Possible Surgery
 25% good neuro outcome
Crit Care Med 2000;28:1556 Neurology 2008;70:1023

26. Acute herniation: Brain Code!
 1. Hyperventilate
 2. Augment BP
 3. Osmotherapy
 Mannitol 1-1.5g/kg
 23.4% 0.5cc/kg slow IV push (slow! 5-10 min)
 Identify underlying process
 Initiate long-term strategies: “stepwise
approach” to intracranial hypertension

27. ICP

28. Monroe – Kellie Doctrine
 Cranial vault is fixed
in size
 Brain volume and
arterial blood volume
do not change
 Venous blood and
CSF reflect the
capacitance of the
system
ICP CompensationICP Compensation

29. ICP waveforms
 During conditions
of decreased IC
compliance, the
second / third
elements of the ICP
wave become
increased
 Often noted prior to
elevation of ICP
aveformsaveforms

30. ICP and CPP
 CPP = MAP-ICP
 65-5 = 60
 65-35 = 30…BUT
95-35 = 60
 When CPP is low,
reflex vasodilation
increases CBV
 ↑CBV → ↑ICP
 This “spiral” causes
plateau waves
Keep CPP> 50mmHg!

31. SURGICAL DECOMPRESSION
SEDATION
CPP OPTIMIZATION
OSMOTHERAPY
HYPERVENTILATION
PENTOBARBITAL
HYPOTHERMIA7
6
5
4
3
2
1
Columbia
Stepwise ICP
Protocol

32. Management of ICP: CPP
optimization
 Vasopressors
increase MAP and
improve both CPP
and metabolic
indices of perfusion
 BP is not equal to
CBF – verify with
functional
evaluation of CO/CI
“look ma, no mannitol”

33. Management of ICP -
Osmotherapy
 Mannitol
 Standard therapy
 1-1.5 mg/kg IV infusion
 Osmotic diuretic
 Pseudohyponatremia
 Follow serum osms to
prevent ARF (<320)
 Hypertonic saline
(23.4%)
 30-60cc bolus
 Volume expander
 Rapid increase in preload
 10-20% incidence transient
hypotension
 Hypertonic saline (3%
infusion)
 Hypernatremia
 Salt and volume overload
 Associated with VAP, CHF

34. Management of ICP –
hyperventilation causes ischemia
 Decreased pCO2 causes rapid
cerebral arteriolar constriction
 Decreased CBF and CBV
cause a decrease in ICP
 Brief hyperventilation, weaned
over 3-6 hours, is standard with
herniation syndromes, but…
 Prolonged hyperventilation
associated with brain ischemia
 Low normal may help a lot!

35. Management of ICP -
Pentobarbitol
 Metabolic therapy:
 Decreases CMRO2
 Decreases CBF
 Powerful, rapid effect
on ICP
 Unclear duration of
infusion
 5-20 mg/kg bolus
followed by 1-
4mg/kg/hr
 Adverse effects:
 Loss of exam
 Deep, prolonged
sedation
 Infection
 Cardiac dysfunction
 Unclear effect on
outcomes

36. Management of ICP -
Hypothermia
 Metabolic therapy
 Decreases CMRO2
 35ºC or 33ºC
 Must suppress shivering
 Caution regarding infections
 Especially in conjunction with
barbiturates
 Prophylactic hypothermia
after TBI is associated with
WORSE outcome

37. What works for ICP?

38. Spinal fluid leak
 Due to disruption of meninges
 Skull fracture, postop, spontaneous
 Can lead to intracranial hypotension,
herniation, brain sag, subdural hematoma,
terrible headache, etc
 Infection risk (meningitis)
 Often treated (paradoxically) by FLAT
positioning and CSF diversion

39. Brain tissue oxygen monitoring
 ICP/CPP based-therapy
alone or ICP/CPP/PbtO2
based therapy?
 Many centers moving to
PbtO2 monitoring
 BOOST-III now underway!

40. Diffuse axonal injury (DAI)
 Scan doesn’t look
bad, exam is bad
 Injury is at the
microscopic level –
axons of neurons are
torn
 Cell bodies die
 No test is very good
to establish
diagnosis – MRI as
shown – other
causes excluded
 Beware mimics…
Gasparotti - Insights Imaging (2011)

41. WHAT SHOULD WE DO?

42. BTF Guidelines
 28 recommendations
 1 level 1
 7 level IIa
 10 level IIb
 10 level III
 Not that helpful…

43. BTF Guidelines
 Bifrontal DHC does not improve outcomes, but
decreases ICP and ICU LOS (IIa)
 Large DHC is better than small DHC (IIa)
 Prophylactic hypothermia not recommended for
patients with diffuse injury (IIb)
 Continuous drainage of CSF reduces ICP more
than intermittent drainage (III)
 CSF drainage to lower ICP may be considered in
patients with GCS<6) (III)

44. BTF Guidelines
 Prolonged hyperventilation not recommended (IIb)
 Barbiturates to prevent ICP elevation not
recommended
 Barbiturates are recommended to control refractory
ICP elevation
 Corticosteroids increase mortality and do not help
control ICP
 Feed patients ≤ day 5 and not after day 7 decreases
mortality (IIa)
 Transgastric jejunal feeds are recommended (IIb)

45. BTF Guidelines
 Early tracheostomy reduces duration of
mechanical ventilation but not mortality
 Antimicrobial EVDs may reduce infection
 Consider early (7d) seizure prophylaxis
 ICP monitoring recommended in Severe TBI
to reduce early mortality
 GCS 3-8 with abnormal CT scan (mass effect)
 Or, age >40, posturing, or SBP<90mmHg

46. BTF Guidelines
 SBP>100 (age 50-69)
 SBP> 110 (AGE 18-49, or > 70)
 Treat ICP > 22mmHg
 Target CPP 60-70
 No compelling data for a specific form of
DVT prophylaxis

47. Test Prep: What should you
study?
 Anatomy:
 Basic neuroanatomy, brainstem, function of
cerebral hemispheres, motor and sensory
pathways, blood and CSF circulation
 LOC, Motor exam, sensory exam
 Integration: Deficits caused by specific
lesions
 Cerebral autoregulation

48. Test Prep: What should you
study?
 ICP, CPP, Monroe-Kellie doctrine
 How to manage ICP elevation
 Primary
 HOB up and neck midline, CSF drainage, ventilation to
pCO2 30-35, CPP 50-70mmHg, normothermia
 Secondary
 Mannitol
 Hypertonic saline
 Tertiary
 Surgery, hypothermia, barbiturates

49. Test Prep: What should you
study?
 Types of traumatic brain injuries
 Where in the brain
 Usual complications
 Usual management
 Hospital course
 Seizures
 Primary problem or a complication of all other
brain injuries

50.  Brain death
 History
 Neurological examination
 Apnea testing
 Some patients may require confirmatory
neuroimaging
 Glasgow Coma Scale
Test Prep: What should you
study?

51. Cases / Practice questions
 45 yo♂ with HA, R arm and facial weakness,
aphasia: where’s the lesion?
 R parietal lobe
 L temporal lobe
 R frontal lobe
 L frontal lobe

52. Cases / Practice questions
 64 yo♀ presented 4h prior with SDH –
evacuated. ICP monitor now shows ICP
24mmHg, MAP is 88. After draining CSF,
the most appropriate intervention is:
 Lower HOB
 Give osmotherapy
 Pentobarbitol coma
 Hyperventilate to pCO2 28

53. Cases / Practice questions
 34♂ yo severe TBI – on day 4 UOP increases
to 1000cc/hr. MAP decreases to 75mmHg
and ICP increases to 30mmHg. What is the
next intervention?
 500cc IVF
 50g mannitol
 Nicardipine infusion
 No intervention – numbers look OK.

54. Cases / Practice questions
 24 yo♂ with epidural hematoma and diffuse
petechial hemorrhages on CT after severe TBI.
GCS 1-3-1. To OR – returns with ICP/PbtO2
monitor: MAP 80, ICP 10, CPP 70, PbtO2 12,
PCO2 26, CVP 10. What is your intervention?
 250cc NS
 Mannitol 25gm
 Decrease Vt or RR to increase PCO2
 Nothing – data look OK

55. QUESTIONS?