6 Cerebral Edema and Elevated Intracranial Pressure

Anna Karpenko and Michelle Ghobrial

Abstract

Elevated intracranial pressure (ICP) is a medical condition commonly encountered in the intensive care unit (ICU) and can be seen in association with several highly morbid processes including traumatic brain injury, global hypoxic injury, large territory strokes, intracranial hemorrhage, brain tumor, and hepatic encephalopathy among other etiologies. In this chapter, we will discuss the stepwise management of elevated ICP.

cerebral edema – intracranial pressure – cerebral perfusion pressure – management – therapeutic temperature management – hyperosmolar therapy

6 Cerebral Edema and Elevated Intracranial Pressure

6.1 The basics

6.1.1 Monro-Kellie doctrine

(Fig. 6‑1)

There is a fixed volume within the cranial vault consisting of:
- Blood (arterial and venous), 10%
- Cerebrospinal fluid (CSF), 10%
- Brain parenchyma, 80%
An increase in any one will lead to a decrease in the other two
- Example: intracranial tumor will take up space at the expense of CSF and blood volume which can lead to elevated intracranial pressure (ICP) and decreased blood flow

6.1.2 ICP and cerebral perfusion pressure (CPP)

Normal ICP in adults is 5 to 15 mm Hg
CSF is produced and reabsorbed in a continuous fashion. The body produces approximately 500 mL/day.
CPP = MAP – ICP
Normal CPP is 50 to 90 mm Hg
Cerebral autoregulation (Fig. 6‑2) allows cerebral blood flow to be maintained across a range of cerebral perfusion pressures (50–150 mm Hg)
Intracranial hypertension is defined as sustained ICP >20 mm Hg
- ICP elevation is independent risk factor for poor outcome in brain trauma ⁵
- Table 6‑1 lists some of the more common causes of elevated ICP
Indications for ICP monitoring
- Obstructive hydrocephalus
- Communicating hydrocephalus with early signs of high ICP
- Severe traumatic brain injury (TBI) patients
- ICP monitors are addressed within Chapter 17

**Fig. 6.2** Cerebral autoregulation curve. In a normal brain, varying the size of the blood vessel allows the brain to maintain a constant cerebral blood flow over a range of cerebral perfusion pressures (50–150mm Hg). When the cerebral perfusion pressure (CPP) is > 150mm Hg (hyperemic state), blood vessels become “leaky.” There is blood– brain barrier breakdown and endothelial injury causing cerebral edema. On the other end, when the CPP is > 50mm Hg (reactive vasodilation), the vessels are maximally dilated and blood flow continues to fall causing hypoperfusion and ischemia. On both ends there is an increase in intracranial pressure (ICP) when autoregulation is disrupted. (Reproduced with permission from Rose J.C. et al. Optimizing blood pressure in neurological emergencies. Springer Nature Jan 1, 2004.)

**Table 6.1** Conditions associated with elevated intracranial pressure
Brain tumor	Meningitis/Encephalitis
Traumatic brain injury	Fulminant hepatic failure
Hemispheric stroke	Eclampsia
Subarachnoid hemorrhage	Hypertensive encephalopathy
Anoxic brain injury	Subdural, epidural, or intracranial hemorrhage

6.1.3 Intracranial compliance

(Fig. 6‑3)

Intracranial compliance is defined as the change in volume over the change in pressure (ΔV/ΔP) ¹
With increase in intracranial volume
- ICP slowly increases
- CSF displaces into the thecal sac
- Decrease in venous return from compression of the cerebral veins
- Without intervention ICP becomes malignant and deadly

6.1.4 ICP Waveforms and Herniation Syndromes

With ICP monitoring, it is common to review the waveform at the bedside
Three components to the ICP waveform (Fig. 6‑4)
- P1: percussive wave represents arterial pulsation transmitted through the choroid plexus to the CSF
- P2: tidal wave represents cerebral compliance
- P3: dicrotic wave represents closure of aortic valve (venous outflow)
When P2 is elevated above P1 it is a sign of poor intracranial compliance (Fig. 6‑5) and that management is needed
Pathologic ICP waveforms ⁴ ^, ⁵ ^, ⁶ (Lundberg waves) (Fig. 6‑6)
- Occur when ICP is increased and intracranial compliance is decrease
- Three waveforms that occur
  - Lundberg A: sustained elevated ICP that needs immediate treatment
  - Lundberg B: unstable ICP and should be aggressively managed
  - Lundberg C: clinically insignificant
Herniation syndromes ⁷ ^, ⁸ (Table 6‑2; Fig. 6‑7)
- Brain herniation occurs when pressure gradients cause the brain parenchyma to shift displacing and compressing surrounding tissues, cranial nerves, and blood vessels
- Note that herniation occurs in approximately one-third of patients without elevated ICP

**Fig. 6.4** Normal intracranial pressure waveforms. (Adapted from Abraham M and Singhal V. Intracranial Pressure Monitoring. Journal of Neuroanaesthesiology and Critical Care. Thieme 2015.)

**Fig. 6.5** Pathologic waveforms indicating poor compliance. (Adapted from Abraham M and Singhal V. Intracranial Pressure Monitoring. Journal of Neuroanaesthesiology and Critical Care. Thieme 2015.)

**Fig. 6.6** Lundberg waves. Lundberg A waves, “Plateau waves,” represent sudden increased in intracranial pressure (ICP) > 20 mm Hg for >5 minutes; sign of impending herniation. Lundberg B waves, “Pressure Waves,” are smaller increases in ICP for shorter period of time; self-limited associated with vasomotor changes and unstable ICP. Lundberg C waves are low amplitude period waves. They occur every 4 to 8 minutes and are of unknown significance. (From Hirzallah MO, Choi HA. The Monitoring of Brain Edema and Intracranial Hypertension. J Neurocit Care 2016;9:92–104.)

**Fig. 6.7** Brain herniation subtypes: (a) Subfalcine, (b) Central, (c) Uncal, (d) Upward/Tonsillar. (Reproduced with permission from ICP management. In Jallo G, Kothbauer K, Recinos V. ed, Handbook of Pediatric Neurosurgery. 1st edition. Thieme; 2018.)

**Table 6.2** Herniation syndromes
Syndrome	Clinical finding
Uncal herniation	Ipsilateral fixed and dilated pupil due to 3rd nerve palsy Can be signs of confusion or agitation prior to pupil change Motor posturing contralateral or bilateral
Subfalcine (Cingulate) herniation	Can be asymptomatic until the anterior cerebral artery is compressed Decreased mental status Contralateral leg weakness
Central (Transtentorial) herniation There are stages of herniation Diencephalic Midbrain-upper pons Power pons-upper medullary Medullary (terminal)	Diabetes insipidus due to shearing of the pituitary stalk Cortical blindness from entrapment of the posterior cerebral arteries Altered consciousness → coma Bilateral pupil dilation Extensor motor posturing Respiratory changes (not normally seen on mechanically ventilated patients)
Upward herniation	Bilateral pupillary dilation Extensor posturing Altered consciousness → coma
Cerebellar (Tonsillar) downward herniation	Altered consciousness → coma Respiratory arrest Cardiac arrhythmias
External or transcalvarial herniation Post decompressive surgery Due to skull fracture	Symptoms depend on area affected

6.2 Cerebral Edema

Common complication for patients in the neurologic intensive care unit (ICU)
Approximately half of the patients will develop increase in ICP or cerebral edema requiring intervention
There are two types of cerebral edema:
- Vasogenic edema
  - Breakdown of blood–brain barrier
  - Increased fluid within the extracellular space
  - Commonly associated with:
    - Brain tumor
    - Infection: Meningitis, encephalitis, abscess
    - Cerebral contusion
  - Affects white matter rather than grey matter within the brain. On imaging there is preservation of the grey–white junction.
  - Managed mostly with glucocorticoids and mannitol
  - Cytotoxic edema
  - Intracellular accumulation of fluid; metabolic changes within the cell
  - Swelling of cells
  - Commonly associated with
    - Stroke
    - Liver failure
    - Water intoxication
  - Affects grey and white matter within the brain with loss of the grey–white junction on imaging
  - Managed primarily with hyperosmolar medications, not responsive to glucocorticoids