1. Intracranial Hypertension
Andreia Cage RN, MSN, ANP-BC, ACNP-BC

2. Objectives
Upon completion of this presentation the participants will be able to:
Discuss the physiology of intracranial hypertension.
Recognize the clinical manifestations of intracranial hypertension.
Identify indications for intracranial pressure monitoring.
Identify specific causes of intracranial hypertension.
Employ general management measures in the treatment of intracranial hypertension.

3. Intracranial Physiology

4. Normal Brain Monro-Kellie hypothesis Blood Brain CSF
In adults the intracranial compartment is protected by the skull
There is a fixed internal volume of mL

5. Intracranial pressure volume relationship
Poor compliance
High compliance
Volume

6. Compensatory mechanisms

7. Compensatory Mechanisms

8. Regulation of Cerebral Blood Flow
Oxygen
CO2
Metabolism
Cerebral perfusion pressure
(CPP = MAP - ICP)

9. Relationship between O2 and CBF
The brain uses ~ 20% of available O2 for functioning
CBF in increased with paO2 < 50mmHg
Cerebral blood flow increases maintain cerebral oxygen delivery (CDO2 )

10. Relationship between CO2 and CBF
Hyperventilation is one known method of rapidly lowering ICP
Decreased PaCO2 leads to arterial vasoconstriction thus lowering CBF, cerebral blood volume, and ICP
Although the effects of hyperventilation are almost immediate, these effects on CBF diminish over 6-24 hours as the brain adapts by changing bicarbonate levels in the extracellular fluid to normalize the pH
CBF
paCO2

11. Relationship between brain metabolism and CBF
The brain receives ~ 25% of the total body glucose
Adenosine triphosphate (ATP) is the most important energy source for the brain
The end product of anaerobic glycolysis is lactic acid
Lactic acid is toxic to neurons and decreases the pH

12. Relationship between brain metabolism and CBF in the injured brain
Decreased CBF is frequently seen following severe head injury
It is thought to be secondary to depressed metabolism
Positron emission tomography studies within 8–14 hours of injury show reduced CBF and global cerebral metabolic rate of oxygen (CMRO2)

13. Relationship of Cerebral Perfusion Pressure and CBF
CPP= MAP-ICP
A reduction in CPP can result in devastating focal or global ischemia
Excessive elevation in CPP can lead to hypertensive encephalopathy and cerebral edema
A higher CPP is tolerated in patients with chronic hypertension because the autoregulatory curve is shifted to the right
Autoregulation is responsible for maintaining CBF at a relatively constant level by cerebrovascular autoregulation of Cerebral Vascular Resistance (CVR) over a wide rage of cerebral perfusion pressures of mmHg

14. Relationship of Cerebral Perfusion Pressure and CBF

15. What is intracranial hypertension?
Elevated pressure within the cranial vault
Defined as ICP >20 mmHg
As Dr. Diringer would say, “It is the ultimate compartment syndrome!”

16. Why is intracranial hypertension so important?
Without prompt recognition of elevated ICPs it WILL lead to
Decreased cerebral perfusion
Ischemia
Infarction
Permanent neurologic disability
Herniation
Death

17. What causes Intracranial Hypertension?
Intracranial mass lesions
Cerebral edema
Hydrocephalus
Idiopathic intracranial hypertension

18. Herniation syndromes 1. Uncal 2. Central 3. Subfalcine
4. Transcalvarial
5. Infratentorial
6. Tonsillar

19. Pressure gradients and shift
The cranial vault is divided into compartments by the dural reflections of the falx cerebri and the tentorium cereblli
Elevated ICP frequently results in pressure gradients between compartments and a shift of brain structures
Lateral displacement of the pineal gland correlates with LOC

20. Clinical manifestations of elevated ICP
Nausea/vomiting
Headache
Altered LOC
Papilledema
Anisocoria
Seizures
Posturing
Cushing’s Triad
Widened pulse pressure
Bradycardia
Abnormal respiratory pattern

21. Papilledema

22. Clinical signs of herniation

23. CT images of herniation syndromes
Subfalcine herniation
Uncal herniation

24. CT images of herniation syndromes
Downward transtentorial
Tonsillar herniation

25. Rationale for ICP monitoring
Elevated ICP can contribute to secondary injury
Reduces cerebral perfusion pressure (CPP) leading to global hypoperfusion and ischemia
Routine ICP monitoring may be used for
Detection of delayed hematoma
Monitoring sedated patients
Determining prognosis

26. Indications for ICP monitoring
GCS <9 and with an abnormal CT scan
Comatose patients with normal CT scan and two or more of the following;
Age >40
Posturing
SBP <90

27. Types of ICP monitors Intraparenchymal Subarachnoid Intraventricular
Epidural

28. ICP waveforms P1 = (Percussion wave) represents arterial pulsation
P2 = (Tidal wave) represents intracranial compliance
P3 = (Dicrotic wave) represents aortic valve closure

29. Treatment of intracranial hypertension

30. Positioning HOB elevated Head in neutral position
Avoid tight C-collars

31. Hyperventilation Acute hyperventilation reduces ICP
Cerebral vasoconstriction (due to rise in CSF pH)
 Cerebral blood flow (CBF)
 Cerebral blood volume (CBV)
 Intracranial pressure (ICP)
Effects are temporary!

32. Metabolic consequences of hyperventilation
CBF falls
In order to maintain constant oxygen delivery, extraction rises
Over several hours CSF pH returns to normal producing vasodilation returning CBF and CBV to baseline

33. Weaning hyperventilation
After several hours of sustained HV CSF pH returns to normal
Any reduction in minute ventilation results in cerebral vasodilation
Impact on ICP depends on intracranial compliance

34. Mannitol & Hypertonic Saline

35. Osmotic therapy Mannitol and hypertonic saline:
Reverse clinical herniation, even with normal ICP
Reduces ICP
Thought to work due to osmotically induced fluid shifts

36. Hemodynamic effects Both agents
Initial  blood volume, cardiac output and BP
Mannitol only
Rapidly followed by diuresis which can lead to hypovolemia

37. Mannitol Therapy Rapidly deteriorating patient IV bolus 1-1.5gm/kg
Followed by gm/kg q 6 hrs.
Requires BMP and serum osmolality q 12 hrs.

38. Brain Relaxation/Dehydration
Osmotic gradient with mannitol appears to draw intracellular fluid from brain to serum
Mannitol
H2O
Blood Brain
Blood Brain
Blood Brain
H2O
H2O
Normal equilibrium
Mannitol infusion
Mannitol equilibrium
Wu C-T, et al. Anes Analges 2010; 110:
Rozet I, et al. Anesthes 2007; 107:

39. Impact of Cerebral Autoregulation
Immediate effect of mannitol is plasma expansion
Augmented blood volume increases cerebral blood flow
Compensatory vasoconstriction
H2O
Normal equilibrium
Mannitol infusion
Vasoconstriction

40. Potential complications of Mannitol
Mannitol accumulation in damaged brain
Rebound edema
Renal failure
Mannitol leakage

41. Mannitol leakage HS always enter brain interstitial fluid
Mannitol enters brain interstitial fluid if blood-brain-barrier disrupted
Does it stay?

42. MRI imaging of Mannitol
Pre-dialysis
Post-dialysis

43. Mannitol therapy Must calculate osmotic gap
Difference between serum osmolality and calculated serum osmolality
Calculated osmolality = (Na x 2) + (BUN/2.8) + (glucose/18)

44. Use of the osmotic gap
Osmotic gap – difference between measured and calculated osmolality
Identifies unmeasured osmoles such as Mannitol or ethanol
Measure as “trough” to ensure Mannitol excretion is complete
Garcia-Morales et al., Crit Care Med. 2004;32(4):986-91

45. Retrospective review of 110 patients receiving Mannitol
Urine volume routinely replaced
Mannitol dose adjusted if osmotic gap rises
11% incidence of renal insufficiency
No relationship to osmolality or osmotic gap
Renal insufficiency predicted by chronic insults to kidneys (DM, HTN)
Gondim et al. J Neurosurg. 2005;103(3):444-7

46. Hypertonic saline 23.4% Equally as effective as Mannitol
Requires central access
0.686 ml of 23.4% saline is equiosmolar to 1gm of Mannitol 5%
3.2mls/kg
Does not require a central line for emergent dose

47. Mannitol vs. Hypertonic saline
Hypertonic saline & mannitol have been compared in a few clinical trials
2 recent meta-analyses compared efficacy
Theoretical benefits of hypertonic saline
Less volume (23.4%)
Lack of diuretic effect
Reflection coefficient (1 vs 0.9)
Attenuation of macrophage & neutrophil activation
Variable immune response
Kamel H, et al. Crit Care Med 2011; 39:
Mortazavi MM, et al. J Neurosurgery 2012; 116:

48. Mannitol vs. Hypertonic saline
Many studies suggest HTS is as good, perhaps better, at reducing ICP compared to mannitol
No clear benefits for:
Safety (except maybe hypotension)
Neurologic outcome
Mortality

49. Therapeutic hypothermia
Rationale –reduces cerebral metabolism
Reduces infarct volume in animals
Appears safe in patients
Very invasive - requires intubation, sedation, paralysis
Reduces ICP

50. Therapeutic hypothermia
Potential complications
Coagulation disorders
Cardiac arrhythmias
Electrolytes shifts
Myocardial depression
Infections
primarily pneumonia

51. Therapeutic hypothermia- techniques

52. Therapeutic hypothermia
Applications
Severe head injury
Large cerebral infarction
Cardiac arrest
Neonatal IVH

53. Early decompressive craniectomy for severe penetrating and closed head injury
Bell RS, Neurosurg Focus, 2010 vol 28, Number 5

54. References http://radiopaedia.org/cases/monro-kellie-hypothesis
American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 1 March 2016 Vol. 310 no. 5, R398-R413 DOI: /ajpregu
Cipolla MJ. The Cerebral Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; Chapter 5, Control of Cerebral Blood Flow. Available from:
Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma 2007; 24 Suppl 1:S37.
Journal of Neurosurgery (Impact Factor: 3.74). 09/ DOI: /jns
Critical Care Medicine: April Volume 32 - Issue 4 - pp
doi: /01.CCM
Li, M., Chen, T., Chen, S., Cai, J., & Hu, Y. (2015). Comparison of Equimolar Doses of Mannitol and Hypertonic Saline for the Treatment of Elevated Intracranial Pressure After Traumatic Brain Injury: A Systematic Review and Meta-Analysis. Medicine, 94(17), e668.