1. Sophia R. Smith, MD WRAMC November 2, 2005
ICP & Head Trauma
Sophia R. Smith, MD
WRAMC
November 2, 2005

2. Introduction
Head injuries are one of the most common causes of disability and death in children.
The Centers for Disease Control and Prevention (CDC) estimates that more than 10,000 children become disabled from a brain injury each year.
Head injuries can be defined as mild as a bump to severe in nature.

3. Prevalence of Pediatric Trauma
Trauma is the leading cause of death in infants and children
Trauma is the cause of 50% of deaths in people between 5 and 34 years of age
Motor vehicle related accidents account for 50% of pediatric trauma cases
$16 billion is spent annually caring for injuries to children less than 16 years of age

4. Traumatic Brain Injury
Primary Brain Injury
Results from what has occurred to the brain at the time of the injury
Secondary Brain Injury
Physiologic and biochemical events which follow the primary injury

6. Examples of Primary Brain Injuries

7. Factors that Effect Secondary Brain Injuries
Blood Pressure
Oxygenation
Temperature
Control of Blood Glucose
Fluid Volume Status
Increased Intracranial Pressure

8. SOME of the SECONDARY EVENTS IN TRAUMATIC BRAIN INJURY
diffuse axonal
injury
inflammation
BBB
disruption
apoptosis
necrosis
edema
formation
Brain trauma
ischemia
energy failure
cytokines
Eicosanoids
endocannabinoids
Calcium
polyamines
Acetyl
Choline
ROS
Shohami, 2000
Green – pathophysiological processes; Yellow – various mediators

9. Anatomy of the cranium
There are various brain contents that are localized within a rigid structure.
Cranium
The cranial vault contents include:
The brain
The cerebral spinal fluid
The cerebral blood

10. Cerebral Spinal Fluid CSF 150 cc in adults at all times
Children slightly less
Produced by choroid plexus – 20 cc/hr
CSF is absorbed into venous system at the subarachnoid villi

11. Cerebral blood and brain
Sum of blood in capillaries, veins, and arteries
Brain
80% of the total intracranial volume
All of these contents are a balanced pressure referred to as intracranial pressure (ICP)

12. Monro-Kellie Doctrine
The ICP within the skull is directly related to the volume of the contents.
Defined as the Monro-Kellie Doctrine
This doctrine states that any increase in volume of the contents within the brain must be met with a decrease in the other cranial contents.

13. Monro-Kellie Doctrine
Vintracranial vault=Vbrain+Vblood +Vcsf

14. Increased Intracranial Pressure

15. Cerebral Blood Flow
CBF is directly linked to the metabolic requirements of the brain.
As the brain metabolic activity increases, CBF increases
Vasodilatation of cerebral vessels
Increase in cerebral blood volume
Consequent increase in ICP

16. Cerebral blood flow CBF maintained when MAP range is 50mmHg to 150mmHg
Cerebral auto regulation
As BP increase baroreceptors sense event and cerebral arteries vasoconstrict CBF maintained with a CBV decrease
As BP decrease  cerebral arteries dilate to increase flow  CBV increase

17. Auto regulation This process is lost in pathological states
Esp. Head trauma
CBF decreases linearly to MAP below range
Results is ischemia (strokes) to brain regions
CBF increases linearly to MAP above auto regulation range
HTN encephalopathy as CBV and ICP increase

19. Mediators of CBF
Local and global mediators of CBF and metabolism are important.
Hypoxia and pH are most important
As local paO2 decreases, CBF increases
CBF is affected by pH (and its surrogate pCO2)

20. Blood: Cerebral Blood Flow
The brain has the ability to control its blood supply to match its metabolic requirements
Chemical or metabolic byproducts of cerebral metabolism can alter blood vessel caliber and behavior

21. Studies of hyperventilation & ICP
This relationship has been well studied as a therapeutic option in particular intentional hyperventilation to lower cerebral blood flow and thus intracranial pressure.
No longer a practice
Modest hyperventilation

22. On call
So, you are in the ER on your first night of call and the next thing you know you get your very first trauma patient.
How do you evaluate?

23. Trauma

24. Traumatic Brain Injury

25. Glascow Coma Scale
Eye Opening      Spontaneous                     4      To Voice                            3      To Pain                               2      None                                  1 Best Verbal      Oriented                             5      Confused                            4      Inappropriate Words           3      Incomprehensible Sounds  2      None                                   1 Best Motor      Obeys Commands              6      Localizes Pain                     5      Withdraws to Pain               4      Flexion to Pain                    3      Extension to Pain                2      None                                   1

27. Severe TBI Indications for Intubation GCS< 8 Fall in GCS of 3
Unequal pupils
Inadequate respiratory effort or significant lung/chest injury
Loss of gag
apnea

28. Treatment
Intubation.
Pretreatment with lidocaine 1 mg/kg IV may prevent rise in intracranial pressure (ICP).

29. Treatment Hyperventilation
to maintain PO2 >90 torrs, PCO2 30 to 32 torrs.
Hyperventilation may actually increase ischemia in at risk brain tissue if PCO2 <25 torr by causing excessive vasoconstriction and has fallen out of favor. Prophylactic hyperventilation for those without increased ICP is contraindicated and worsens outcomes.
PEEP relatively contraindicated because reduces cerebral blood flow.

30. Maintain normal cardiac output.
If hypotensive from other cause such as multi-trauma, treat shock as usual.
Normal saline is preferred over LR since LR is slightly hypotonic.
Hypertonic saline (3% or 7.5%) can be used. Especially if you see ICP changes.

31. Maintain normal cardiac output.
If markedly hypertensive, consider labetalol or nitroprusside.
Avoid lowering the blood pressure unless diastolic blood pressure is >120 mm Hg.

32. Diuresis Mannitol 1 g/kg IV over 20 minutes induces osmotic diuresis.
Avoid if hypotensive or have CHF/renal failure.
Some suggest furosemide (Lasix and others).
Avoid if hypotensive.

33. ICP Precautions Elevate head of bed 30 degrees.
Seizure prophylaxis: Phenytoin will reduce seizures in the first week after injury but does not change the overall outcome.
Steroids are ineffective in controlling ICP in the trauma setting.

34. Positioning II

35. Manipulation of CPP CPP = MAP - ICP
Maintain adequate intravascular volume
CVP
Increase MAP
Utilize alpha agonist--dopamine, phenylephrine, norepinephrine
What is appropriate goal for children?

36. CPP for children Aim for a CPP of >60 mmHg
by maintaining an adequate MAP and control of ICP
MAP – ICP = CPP
Minimizing the morbidity of TBI in children

37. Additional therapies
Prevent hyperglycemia: exacerbates ischemic cerebral damage
Attention to electrolyte status. These patients are prone to electrolyte abnormalities due to osmotic diuresis, cerebral salt losing states, SIADH and diabetes insipidus

38. Manipulation of ICP Blood Decrease cerebral metabolic demand
sedation, analgesia, barbiturates
avoid hyperthermia
avoid seizures
Hyperventilation
decreases blood flow to brain
only acutely for impending herniation
Mannitol

39. Manipulation of ICP Brain Mannitol Hypertonic saline
dehydrate the brain, not the patient!
monitor osmolality
Hypertonic saline
Decompressive craniectomy

40. ICP Monitoring
ICU patients who have sustained head trauma, brain hemorrhage, brain surgery, or conditions in which the brain may swell might require intracranial pressure monitoring.
The purpose of ICP monitoring is to continuously measure the pressure surrounding the brain.

41. Why Monitor? Detect “events” Manage intracranial pressure
Manage cerebral perfusion pressure

42. How? Ventriculostomy Intraparenchymal fiberoptic catheter
Subarachnoid monitor
Useful adjuncts:
Arterial line
Central venous line
Foley catheter

43. Manipulation of ICP CSF External drainage
therapeutic as well as diagnostic
technical issues
infectious issues

44. What to do with the information...
Goal: adequate oxygen delivery to maintain the metabolic needs of the brain.
Intracranial pressure <20
Cerebral perfusion pressure >50-70 mm Hg CPP=MAP-ICP

45. Indications for ICP monitoring
Glasgow coma scale <8
Clinical or radiographic evidence of increased ICP
Post-surgical removal of intracranial hematoma
Less severe brain injury in the setting which requires deep sedation or anesthesia

46. Other monitoring devices
CT Scan
MRI
PET Scan
Jugular Venous Oxygen Saturation

47. Near-infrared Spectroscopy
Uses absorption characteristics of oxy Hgb, deoxy Hgb, and [o] cyt aa3
Uses the ability to penetrate the superficial brain
Therefore the state of oxygenation can be determined.
Good assessment of cerebral oxygenation

48. Transcranial Doppler US
TCD is a noninvasive technique used to determine cerebral blood velocity in large intracranial arteries.
Assessment of
Brain death
Reperfusion injury
Identify regions S/P TBI that are adversely effected

49. Cerebral Microdialysis
Measuring the partial pressure of oxygen of brain parenchyma and metabolites using microdialysis
Electrode in vulnerable brain region measures O2 concentration
Measures also local brain metabolism